--- _id: '14933' abstract: - lang: eng text: Centrioles are part of centrosomes and cilia, which are microtubule organising centres (MTOC) with diverse functions. Despite their stability, centrioles can disappear during differentiation, such as in oocytes, but little is known about the regulation of their structural integrity. Our previous research revealed that the pericentriolar material (PCM) that surrounds centrioles and its recruiter, Polo kinase, are downregulated in oogenesis and sufficient for maintaining both centrosome structural integrity and MTOC activity. We now show that the expression of specific components of the centriole cartwheel and wall, including ANA1/CEP295, is essential for maintaining centrosome integrity. We find that Polo kinase requires ANA1 to promote centriole stability in cultured cells and eggs. In addition, ANA1 expression prevents the loss of centrioles observed upon PCM-downregulation. However, the centrioles maintained by overexpressing and tethering ANA1 are inactive, unlike the MTOCs observed upon tethering Polo kinase. These findings demonstrate that several centriole components are needed to maintain centrosome structure. Our study also highlights that centrioles are more dynamic than previously believed, with their structural stability relying on the continuous expression of multiple components. acknowledgement: We thank all members of the Cell Cycle and Regulation Lab for the discussions and for the critical reading of the manuscript. We thank Tomer Avidor-Reiss (University of Toledo, Toledo, OH), Daniel St. Johnston (The Gurdon Institute, Cambridge, UK), David Glover (University of Cambridge, Cambridge, UK), Jingyan Fu (Agricultural University, Beijing, China) Jordan Raff (University of Oxford, Oxford, UK) and Timothy Megraw (Florida State University, Tallahassee, FL) for sharing tools. We acknowledge the technical support of Instituto Gulbenkian de Ciência (IGC)‘s Advanced Imaging Facility, in particular Gabriel Martins, Nuno Pimpão Martins and José Marques. We also thank Tiago Paixão from the IGC’s Quantitative & Digital Science Unit and Marco Louro from the CCR lab for the support provided on statistical analysis. IGC’s Advanced Imaging Facility (AIF-UIC) is supported by the national Portuguese funding ref# PPBI-POCI-01-0145-FEDER -022122. We thank the IGC’s Fly Facility, supported by CONGENTO (LISBOA-01-0145-FEDER-022170). This work was supported by an ERC grant (ERC-2015-CoG-683258) awarded to MBD and a grant from the Portuguese Research Council (FCT) awarded to APM (PTDC/BIA-BID/32225/2017). article_processing_charge: Yes (in subscription journal) article_type: original author: - first_name: Ana full_name: Pimenta-Marques, Ana last_name: Pimenta-Marques - first_name: Tania full_name: Perestrelo, Tania last_name: Perestrelo - first_name: Patricia full_name: Dos Reis Rodrigues, Patricia id: 26E95904-5160-11E9-9C0B-C5B0DC97E90F last_name: Dos Reis Rodrigues orcid: 0000-0003-1681-508X - first_name: Paulo full_name: Duarte, Paulo last_name: Duarte - first_name: Ana full_name: Ferreira-Silva, Ana last_name: Ferreira-Silva - first_name: Mariana full_name: Lince-Faria, Mariana last_name: Lince-Faria - first_name: Mónica full_name: Bettencourt-Dias, Mónica last_name: Bettencourt-Dias citation: ama: Pimenta-Marques A, Perestrelo T, Dos Reis Rodrigues P, et al. Ana1/CEP295 is an essential player in the centrosome maintenance program regulated by Polo kinase and the PCM. EMBO reports. 2024;25(1):102-127. doi:10.1038/s44319-023-00020-6 apa: Pimenta-Marques, A., Perestrelo, T., Dos Reis Rodrigues, P., Duarte, P., Ferreira-Silva, A., Lince-Faria, M., & Bettencourt-Dias, M. (2024). Ana1/CEP295 is an essential player in the centrosome maintenance program regulated by Polo kinase and the PCM. EMBO Reports. Embo Press. https://doi.org/10.1038/s44319-023-00020-6 chicago: Pimenta-Marques, Ana, Tania Perestrelo, Patricia Dos Reis Rodrigues, Paulo Duarte, Ana Ferreira-Silva, Mariana Lince-Faria, and Mónica Bettencourt-Dias. “Ana1/CEP295 Is an Essential Player in the Centrosome Maintenance Program Regulated by Polo Kinase and the PCM.” EMBO Reports. Embo Press, 2024. https://doi.org/10.1038/s44319-023-00020-6. ieee: A. Pimenta-Marques et al., “Ana1/CEP295 is an essential player in the centrosome maintenance program regulated by Polo kinase and the PCM,” EMBO reports, vol. 25, no. 1. Embo Press, pp. 102–127, 2024. ista: Pimenta-Marques A, Perestrelo T, Dos Reis Rodrigues P, Duarte P, Ferreira-Silva A, Lince-Faria M, Bettencourt-Dias M. 2024. Ana1/CEP295 is an essential player in the centrosome maintenance program regulated by Polo kinase and the PCM. EMBO reports. 25(1), 102–127. mla: Pimenta-Marques, Ana, et al. “Ana1/CEP295 Is an Essential Player in the Centrosome Maintenance Program Regulated by Polo Kinase and the PCM.” EMBO Reports, vol. 25, no. 1, Embo Press, 2024, pp. 102–27, doi:10.1038/s44319-023-00020-6. short: A. Pimenta-Marques, T. Perestrelo, P. Dos Reis Rodrigues, P. Duarte, A. Ferreira-Silva, M. Lince-Faria, M. Bettencourt-Dias, EMBO Reports 25 (2024) 102–127. date_created: 2024-02-04T23:00:53Z date_published: 2024-01-10T00:00:00Z date_updated: 2024-02-05T12:37:07Z day: '10' ddc: - '570' department: - _id: MiSi doi: 10.1038/s44319-023-00020-6 file: - access_level: open_access checksum: 53c3ef43d9bd6d7bff3ffcf57d763cac content_type: application/pdf creator: dernst date_created: 2024-02-05T12:35:03Z date_updated: 2024-02-05T12:35:03Z file_id: '14941' file_name: 2023_EmboReports_PimentaMarques.pdf file_size: 9645056 relation: main_file success: 1 file_date_updated: 2024-02-05T12:35:03Z has_accepted_license: '1' intvolume: ' 25' issue: '1' language: - iso: eng month: '01' oa: 1 oa_version: Published Version page: 102-127 publication: EMBO reports publication_identifier: eissn: - 1469-3178 publication_status: published publisher: Embo Press quality_controlled: '1' scopus_import: '1' status: public title: Ana1/CEP295 is an essential player in the centrosome maintenance program regulated by Polo kinase and the PCM tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 25 year: '2024' ... --- _id: '14846' abstract: - lang: eng text: Contraction and flow of the actin cell cortex have emerged as a common principle by which cells reorganize their cytoplasm and take shape. However, how these cortical flows interact with adjacent cytoplasmic components, changing their form and localization, and how this affects cytoplasmic organization and cell shape remains unclear. Here we show that in ascidian oocytes, the cooperative activities of cortical actomyosin flows and deformation of the adjacent mitochondria-rich myoplasm drive oocyte cytoplasmic reorganization and shape changes following fertilization. We show that vegetal-directed cortical actomyosin flows, established upon oocyte fertilization, lead to both the accumulation of cortical actin at the vegetal pole of the zygote and compression and local buckling of the adjacent elastic solid-like myoplasm layer due to friction forces generated at their interface. Once cortical flows have ceased, the multiple myoplasm buckles resolve into one larger buckle, which again drives the formation of the contraction pole—a protuberance of the zygote’s vegetal pole where maternal mRNAs accumulate. Thus, our findings reveal a mechanism where cortical actomyosin network flows determine cytoplasmic reorganization and cell shape by deforming adjacent cytoplasmic components through friction forces. acknowledged_ssus: - _id: EM-Fac - _id: Bio - _id: NanoFab acknowledgement: We would like to thank A. McDougall, E. Hannezo and the Heisenberg lab for fruitful discussions and reagents. We also thank E. Munro for the iMyo-YFP and Bra>iMyo-mScarlet constructs. This research was supported by the Scientific Service Units of the Institute of Science and Technology Austria through resources provided by the Electron Microscopy Facility, Imaging and Optics Facility and the Nanofabrication Facility. This work was supported by a Joint Project Grant from the FWF (I 3601-B27). article_processing_charge: Yes (in subscription journal) article_type: original author: - first_name: Silvia full_name: Caballero Mancebo, Silvia id: 2F1E1758-F248-11E8-B48F-1D18A9856A87 last_name: Caballero Mancebo orcid: 0000-0002-5223-3346 - first_name: Rushikesh full_name: Shinde, Rushikesh last_name: Shinde - first_name: Madison full_name: Bolger-Munro, Madison id: 516F03FA-93A3-11EA-A7C5-D6BE3DDC885E last_name: Bolger-Munro orcid: 0000-0002-8176-4824 - first_name: Matilda full_name: Peruzzo, Matilda id: 3F920B30-F248-11E8-B48F-1D18A9856A87 last_name: Peruzzo orcid: 0000-0002-3415-4628 - first_name: Gregory full_name: Szep, Gregory id: 4BFB7762-F248-11E8-B48F-1D18A9856A87 last_name: Szep - first_name: Irene full_name: Steccari, Irene id: 2705C766-9FE2-11EA-B224-C6773DDC885E last_name: Steccari - first_name: David full_name: Labrousse Arias, David id: CD573DF4-9ED3-11E9-9D77-3223E6697425 last_name: Labrousse Arias - first_name: Vanessa full_name: Zheden, Vanessa id: 39C5A68A-F248-11E8-B48F-1D18A9856A87 last_name: Zheden orcid: 0000-0002-9438-4783 - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Andrew full_name: Callan-Jones, Andrew last_name: Callan-Jones - first_name: Raphaël full_name: Voituriez, Raphaël last_name: Voituriez - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 citation: ama: Caballero Mancebo S, Shinde R, Bolger-Munro M, et al. Friction forces determine cytoplasmic reorganization and shape changes of ascidian oocytes upon fertilization. Nature Physics. 2024. doi:10.1038/s41567-023-02302-1 apa: Caballero Mancebo, S., Shinde, R., Bolger-Munro, M., Peruzzo, M., Szep, G., Steccari, I., … Heisenberg, C.-P. J. (2024). Friction forces determine cytoplasmic reorganization and shape changes of ascidian oocytes upon fertilization. Nature Physics. Springer Nature. https://doi.org/10.1038/s41567-023-02302-1 chicago: Caballero Mancebo, Silvia, Rushikesh Shinde, Madison Bolger-Munro, Matilda Peruzzo, Gregory Szep, Irene Steccari, David Labrousse Arias, et al. “Friction Forces Determine Cytoplasmic Reorganization and Shape Changes of Ascidian Oocytes upon Fertilization.” Nature Physics. Springer Nature, 2024. https://doi.org/10.1038/s41567-023-02302-1. ieee: S. Caballero Mancebo et al., “Friction forces determine cytoplasmic reorganization and shape changes of ascidian oocytes upon fertilization,” Nature Physics. Springer Nature, 2024. ista: Caballero Mancebo S, Shinde R, Bolger-Munro M, Peruzzo M, Szep G, Steccari I, Labrousse Arias D, Zheden V, Merrin J, Callan-Jones A, Voituriez R, Heisenberg C-PJ. 2024. Friction forces determine cytoplasmic reorganization and shape changes of ascidian oocytes upon fertilization. Nature Physics. mla: Caballero Mancebo, Silvia, et al. “Friction Forces Determine Cytoplasmic Reorganization and Shape Changes of Ascidian Oocytes upon Fertilization.” Nature Physics, Springer Nature, 2024, doi:10.1038/s41567-023-02302-1. short: S. Caballero Mancebo, R. Shinde, M. Bolger-Munro, M. Peruzzo, G. Szep, I. Steccari, D. Labrousse Arias, V. Zheden, J. Merrin, A. Callan-Jones, R. Voituriez, C.-P.J. Heisenberg, Nature Physics (2024). date_created: 2024-01-21T23:00:57Z date_published: 2024-01-09T00:00:00Z date_updated: 2024-03-05T09:33:38Z day: '09' department: - _id: CaHe - _id: JoFi - _id: MiSi - _id: EM-Fac - _id: NanoFab doi: 10.1038/s41567-023-02302-1 has_accepted_license: '1' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1038/s41567-023-02302-1 month: '01' oa: 1 oa_version: Published Version project: - _id: 2646861A-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: I03601 name: Control of embryonic cleavage pattern publication: Nature Physics publication_identifier: eissn: - 1745-2481 issn: - 1745-2473 publication_status: epub_ahead publisher: Springer Nature quality_controlled: '1' related_material: link: - description: News on ISTA Website relation: press_release url: https://ista.ac.at/en/news/stranger-than-friction-a-force-initiating-life/ scopus_import: '1' status: public title: Friction forces determine cytoplasmic reorganization and shape changes of ascidian oocytes upon fertilization tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2024' ... --- _id: '15146' abstract: - lang: eng text: The extracellular matrix (ECM) serves as a scaffold for cells and plays an essential role in regulating numerous cellular processes, including cell migration and proliferation. Due to limitations in specimen preparation for conventional room-temperature electron microscopy, we lack structural knowledge on how ECM components are secreted, remodeled, and interact with surrounding cells. We have developed a 3D-ECM platform compatible with sample thinning by cryo-focused ion beam milling, the lift-out extraction procedure, and cryo-electron tomography. Our workflow implements cell-derived matrices (CDMs) grown on EM grids, resulting in a versatile tool closely mimicking ECM environments. This allows us to visualize ECM for the first time in its hydrated, native context. Our data reveal an intricate network of extracellular fibers, their positioning relative to matrix-secreting cells, and previously unresolved structural entities. Our workflow and results add to the structural atlas of the ECM, providing novel insights into its secretion and assembly. acknowledged_ssus: - _id: LifeSc - _id: ScienComp - _id: EM-Fac - _id: M-Shop acknowledgement: "Open Access funding provided by IST Austria. We thank Armel Nicolas and his team at the ISTA proteomics facility, Alois Schloegl, Stefano Elefante, and colleagues at the ISTA Scientific Computing facility, Tommaso Constanzo and Ludek Lovicar at the Electron Microsocpy Facility (EMF), and Thomas Menner at the Miba Machine shop for their support. We also thank Wanda Kukulski (University of Bern) as well as Darío Porley, Andreas Thader, and other members of the Schur group for helpful discussions. Matt Swulius and Jessica Heebner provided great support in using Dragonfly. We thank Dorotea Fracciolla (Art & Science) for support in figure illustration.\r\n\r\nThis research was supported by the Scientific Service Units of ISTA through resources provided by Scientific Computing, the Lab Support Facility, and the Electron Microscopy Facility. We acknowledge funding support from the following sources: Austrian Science Fund (FWF) grant P33367 (to F.K.M. Schur), the Federation of European Biochemical Societies (to F.K.M. Schur), Niederösterreich (NÖ) Fonds (to B. Zens), FWF grant E435 (to J.M. Hansen), European Research Council under the European Union’s Horizon 2020 research (grant agreement No. 724373) (to M. Sixt), and Jenny and Antti Wihuri Foundation (to J. Alanko). This publication has been made possible in part by CZI grant DAF2021-234754 and grant DOI https://doi.org/10.37921/812628ebpcwg from the Chan Zuckerberg Initiative DAF, an advised fund of Silicon Valley Community Foundation (to F.K.M. Schur)." article_number: e202309125 article_processing_charge: Yes (via OA deal) article_type: original author: - first_name: Bettina full_name: Zens, Bettina id: 45FD126C-F248-11E8-B48F-1D18A9856A87 last_name: Zens - first_name: Florian full_name: Fäßler, Florian id: 404F5528-F248-11E8-B48F-1D18A9856A87 last_name: Fäßler orcid: 0000-0001-7149-769X - first_name: Jesse full_name: Hansen, Jesse id: 1063c618-6f9b-11ec-9123-f912fccded63 last_name: Hansen - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Julia full_name: Datler, Julia id: 3B12E2E6-F248-11E8-B48F-1D18A9856A87 last_name: Datler orcid: 0000-0002-3616-8580 - first_name: Victor-Valentin full_name: Hodirnau, Victor-Valentin id: 3661B498-F248-11E8-B48F-1D18A9856A87 last_name: Hodirnau - first_name: Vanessa full_name: Zheden, Vanessa id: 39C5A68A-F248-11E8-B48F-1D18A9856A87 last_name: Zheden orcid: 0000-0002-9438-4783 - first_name: Jonna H full_name: Alanko, Jonna H id: 2CC12E8C-F248-11E8-B48F-1D18A9856A87 last_name: Alanko orcid: 0000-0002-7698-3061 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Florian KM full_name: Schur, Florian KM id: 48AD8942-F248-11E8-B48F-1D18A9856A87 last_name: Schur orcid: 0000-0003-4790-8078 citation: ama: Zens B, Fäßler F, Hansen J, et al. Lift-out cryo-FIBSEM and cryo-ET reveal the ultrastructural landscape of extracellular matrix. Journal of Cell Biology. 2024;223(6). doi:10.1083/jcb.202309125 apa: Zens, B., Fäßler, F., Hansen, J., Hauschild, R., Datler, J., Hodirnau, V.-V., … Schur, F. K. (2024). Lift-out cryo-FIBSEM and cryo-ET reveal the ultrastructural landscape of extracellular matrix. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.202309125 chicago: Zens, Bettina, Florian Fäßler, Jesse Hansen, Robert Hauschild, Julia Datler, Victor-Valentin Hodirnau, Vanessa Zheden, Jonna H Alanko, Michael K Sixt, and Florian KM Schur. “Lift-out Cryo-FIBSEM and Cryo-ET Reveal the Ultrastructural Landscape of Extracellular Matrix.” Journal of Cell Biology. Rockefeller University Press, 2024. https://doi.org/10.1083/jcb.202309125. ieee: B. Zens et al., “Lift-out cryo-FIBSEM and cryo-ET reveal the ultrastructural landscape of extracellular matrix,” Journal of Cell Biology, vol. 223, no. 6. Rockefeller University Press, 2024. ista: Zens B, Fäßler F, Hansen J, Hauschild R, Datler J, Hodirnau V-V, Zheden V, Alanko JH, Sixt MK, Schur FK. 2024. Lift-out cryo-FIBSEM and cryo-ET reveal the ultrastructural landscape of extracellular matrix. Journal of Cell Biology. 223(6), e202309125. mla: Zens, Bettina, et al. “Lift-out Cryo-FIBSEM and Cryo-ET Reveal the Ultrastructural Landscape of Extracellular Matrix.” Journal of Cell Biology, vol. 223, no. 6, e202309125, Rockefeller University Press, 2024, doi:10.1083/jcb.202309125. short: B. Zens, F. Fäßler, J. Hansen, R. Hauschild, J. Datler, V.-V. Hodirnau, V. Zheden, J.H. Alanko, M.K. Sixt, F.K. Schur, Journal of Cell Biology 223 (2024). date_created: 2024-03-21T06:45:51Z date_published: 2024-03-20T00:00:00Z date_updated: 2024-03-25T13:03:57Z day: '20' ddc: - '570' department: - _id: FlSc - _id: MiSi - _id: Bio - _id: EM-Fac doi: 10.1083/jcb.202309125 ec_funded: 1 external_id: pmid: - '38506714' file: - access_level: open_access checksum: 90d1984a93660735e506c2a304bc3f73 content_type: application/pdf creator: dernst date_created: 2024-03-25T12:52:04Z date_updated: 2024-03-25T12:52:04Z file_id: '15188' file_name: 2024_JCB_Zens.pdf file_size: 11907016 relation: main_file success: 1 file_date_updated: 2024-03-25T12:52:04Z has_accepted_license: '1' intvolume: ' 223' issue: '6' language: - iso: eng month: '03' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 9B954C5C-BA93-11EA-9121-9846C619BF3A grant_number: P33367 name: Structure and isoform diversity of the Arp2/3 complex - _id: 7bd318a1-9f16-11ee-852c-cc9217763180 grant_number: E435 name: In Situ Actin Structures via Hybrid Cryo-electron Microscopy - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 059B463C-7A3F-11EA-A408-12923DDC885E name: NÖ-Fonds Preis für die Jungforscherin des Jahres am IST Austria - _id: 2615199A-B435-11E9-9278-68D0E5697425 grant_number: '21317' name: Spatiotemporal regulation of chemokine-induced signalling in leukocyte chemotaxis - _id: 62909c6f-2b32-11ec-9570-e1476aab5308 grant_number: CZI01 name: CryoMinflux-guided in-situ visual proteomics and structure determination publication: Journal of Cell Biology publication_identifier: eissn: - 1540-8140 issn: - 0021-9525 publication_status: published publisher: Rockefeller University Press quality_controlled: '1' scopus_import: '1' status: public title: Lift-out cryo-FIBSEM and cryo-ET reveal the ultrastructural landscape of extracellular matrix tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 223 year: '2024' ... --- _id: '13052' abstract: - lang: eng text: Imaging of the immunological synapse (IS) between dendritic cells (DCs) and T cells in suspension is hampered by suboptimal alignment of cell-cell contacts along the vertical imaging plane. This requires optical sectioning that often results in unsatisfactory resolution in time and space. Here, we present a workflow where DCs and T cells are confined between a layer of glass and polydimethylsiloxane (PDMS) that orients the cells along one, horizontal imaging plane, allowing for fast en-face-imaging of the DC-T cell IS. acknowledged_ssus: - _id: Bio - _id: NanoFab - _id: M-Shop acknowledgement: 'A.L. was funded by an Erwin Schrödinger postdoctoral fellowship of the Austrian Science Fund (FWF, project number: J4542-B) and is an EMBO non-stipendiary postdoctoral fellow. This work was supported by a European Research Council grant ERC-CoG-72437 to M.S. We thank the Imaging & Optics facility, the Nanofabrication facility, and the Miba Machine Shop of ISTA for their excellent support.' alternative_title: - Methods in Molecular Biology article_processing_charge: No author: - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Leithner AF, Merrin J, Sixt MK. En-Face Imaging of T Cell-Dendritic Cell Immunological Synapses. In: Baldari C, Dustin M, eds. The Immune Synapse. Vol 2654. MIMB. New York, NY: Springer Nature; 2023:137-147. doi:10.1007/978-1-0716-3135-5_9' apa: 'Leithner, A. F., Merrin, J., & Sixt, M. K. (2023). En-Face Imaging of T Cell-Dendritic Cell Immunological Synapses. In C. Baldari & M. Dustin (Eds.), The Immune Synapse (Vol. 2654, pp. 137–147). New York, NY: Springer Nature. https://doi.org/10.1007/978-1-0716-3135-5_9' chicago: 'Leithner, Alexander F, Jack Merrin, and Michael K Sixt. “En-Face Imaging of T Cell-Dendritic Cell Immunological Synapses.” In The Immune Synapse, edited by Cosima Baldari and Michael Dustin, 2654:137–47. MIMB. New York, NY: Springer Nature, 2023. https://doi.org/10.1007/978-1-0716-3135-5_9.' ieee: 'A. F. Leithner, J. Merrin, and M. K. Sixt, “En-Face Imaging of T Cell-Dendritic Cell Immunological Synapses,” in The Immune Synapse, vol. 2654, C. Baldari and M. Dustin, Eds. New York, NY: Springer Nature, 2023, pp. 137–147.' ista: 'Leithner AF, Merrin J, Sixt MK. 2023.En-Face Imaging of T Cell-Dendritic Cell Immunological Synapses. In: The Immune Synapse. Methods in Molecular Biology, vol. 2654, 137–147.' mla: Leithner, Alexander F., et al. “En-Face Imaging of T Cell-Dendritic Cell Immunological Synapses.” The Immune Synapse, edited by Cosima Baldari and Michael Dustin, vol. 2654, Springer Nature, 2023, pp. 137–47, doi:10.1007/978-1-0716-3135-5_9. short: A.F. Leithner, J. Merrin, M.K. Sixt, in:, C. Baldari, M. Dustin (Eds.), The Immune Synapse, Springer Nature, New York, NY, 2023, pp. 137–147. date_created: 2023-05-22T08:41:48Z date_published: 2023-04-28T00:00:00Z date_updated: 2023-10-17T08:44:53Z day: '28' department: - _id: MiSi - _id: NanoFab doi: 10.1007/978-1-0716-3135-5_9 ec_funded: 1 editor: - first_name: Cosima full_name: Baldari, Cosima last_name: Baldari - first_name: Michael full_name: Dustin, Michael last_name: Dustin external_id: pmid: - '37106180' intvolume: ' 2654' language: - iso: eng month: '04' oa_version: None page: 137-147 place: New York, NY pmid: 1 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: The Immune Synapse publication_identifier: eisbn: - '9781071631355' eissn: - 1940-6029 isbn: - '9781071631348' issn: - 1064-3745 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' series_title: MIMB status: public title: En-Face Imaging of T Cell-Dendritic Cell Immunological Synapses type: book_chapter user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 2654 year: '2023' ... --- _id: '14555' abstract: - lang: eng text: The intricate regulatory processes behind actin polymerization play a crucial role in cellular biology, including essential mechanisms such as cell migration or cell division. However, the self-organizing principles governing actin polymerization are still poorly understood. In this perspective article, we compare the Belousov-Zhabotinsky (BZ) reaction, a classic and well understood chemical oscillator known for its self-organizing spatiotemporal dynamics, with the excitable dynamics of polymerizing actin. While the BZ reaction originates from the domain of inorganic chemistry, it shares remarkable similarities with actin polymerization, including the characteristic propagating waves, which are influenced by geometry and external fields, and the emergent collective behavior. Starting with a general description of emerging patterns, we elaborate on single droplets or cell-level dynamics, the influence of geometric confinements and conclude with collective interactions. Comparing these two systems sheds light on the universal nature of self-organization principles in both living and inanimate systems. acknowledgement: The author(s) declare that no financial support was received for the research, authorship, and/or publication of this article. article_number: '1287420' article_processing_charge: Yes article_type: original author: - first_name: Michael full_name: Riedl, Michael id: 3BE60946-F248-11E8-B48F-1D18A9856A87 last_name: Riedl orcid: 0000-0003-4844-6311 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Riedl M, Sixt MK. The excitable nature of polymerizing actin and the Belousov-Zhabotinsky reaction. Frontiers in Cell and Developmental Biology. 2023;11. doi:10.3389/fcell.2023.1287420 apa: Riedl, M., & Sixt, M. K. (2023). The excitable nature of polymerizing actin and the Belousov-Zhabotinsky reaction. Frontiers in Cell and Developmental Biology. Frontiers. https://doi.org/10.3389/fcell.2023.1287420 chicago: Riedl, Michael, and Michael K Sixt. “The Excitable Nature of Polymerizing Actin and the Belousov-Zhabotinsky Reaction.” Frontiers in Cell and Developmental Biology. Frontiers, 2023. https://doi.org/10.3389/fcell.2023.1287420. ieee: M. Riedl and M. K. Sixt, “The excitable nature of polymerizing actin and the Belousov-Zhabotinsky reaction,” Frontiers in Cell and Developmental Biology, vol. 11. Frontiers, 2023. ista: Riedl M, Sixt MK. 2023. The excitable nature of polymerizing actin and the Belousov-Zhabotinsky reaction. Frontiers in Cell and Developmental Biology. 11, 1287420. mla: Riedl, Michael, and Michael K. Sixt. “The Excitable Nature of Polymerizing Actin and the Belousov-Zhabotinsky Reaction.” Frontiers in Cell and Developmental Biology, vol. 11, 1287420, Frontiers, 2023, doi:10.3389/fcell.2023.1287420. short: M. Riedl, M.K. Sixt, Frontiers in Cell and Developmental Biology 11 (2023). date_created: 2023-11-19T23:00:55Z date_published: 2023-10-31T00:00:00Z date_updated: 2023-11-20T08:44:17Z day: '31' ddc: - '570' department: - _id: MiSi doi: 10.3389/fcell.2023.1287420 file: - access_level: open_access checksum: 61857fc3ebf019354932e7ee684658ce content_type: application/pdf creator: dernst date_created: 2023-11-20T08:41:15Z date_updated: 2023-11-20T08:41:15Z file_id: '14561' file_name: 2023_FrontiersCellDevBio_Riedl.pdf file_size: 2047622 relation: main_file success: 1 file_date_updated: 2023-11-20T08:41:15Z has_accepted_license: '1' intvolume: ' 11' language: - iso: eng month: '10' oa: 1 oa_version: Published Version publication: Frontiers in Cell and Developmental Biology publication_identifier: eissn: - 2296-634X publication_status: published publisher: Frontiers quality_controlled: '1' scopus_import: '1' status: public title: The excitable nature of polymerizing actin and the Belousov-Zhabotinsky reaction tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 11 year: '2023' ... --- _id: '14530' abstract: - lang: eng text: 'Most motions of many-body systems at any scale in nature with sufficient degrees of freedom tend to be chaotic; reaching from the orbital motion of planets, the air currents in our atmosphere, down to the water flowing through our pipelines or the movement of a population of bacteria. To the observer it is therefore intriguing when a moving collective exhibits order. Collective motion of flocks of birds, schools of fish or swarms of self-propelled particles or robots have been studied extensively over the past decades but the mechanisms involved in the transition from chaos to order remain unclear. Here, the interactions, that in most systems give rise to chaos, sustain order. In this thesis we investigate mechanisms that preserve, destabilize or lead to the ordered state. We show that endothelial cells migrating in circular confinements transition to a collective rotating state and concomitantly synchronize the frequencies of nucleating actin waves within individual cells. Consequently, the frequency dependent cell migration speed uniformizes across the population. Complementary to the WAVE dependent nucleation of traveling actin waves, we show that in leukocytes the actin polymerization depending on WASp generates pushing forces locally at stationary patches. Next, in pipe flows, we study methods to disrupt the self--sustaining cycle of turbulence and therefore relaminarize the flow. While we find in pulsating flow conditions that turbulence emerges through a helical instability during the decelerating phase. Finally, we show quantitatively in brain slices of mice that wild-type control neurons can compensate the migratory deficits of a genetically modified neuronal sub--population in the developing cortex. ' acknowledged_ssus: - _id: M-Shop - _id: Bio alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Michael full_name: Riedl, Michael id: 3BE60946-F248-11E8-B48F-1D18A9856A87 last_name: Riedl orcid: 0000-0003-4844-6311 citation: ama: Riedl M. Synchronization in collectively moving active matter. 2023. doi:10.15479/14530 apa: Riedl, M. (2023). Synchronization in collectively moving active matter. Institute of Science and Technology Austria. https://doi.org/10.15479/14530 chicago: Riedl, Michael. “Synchronization in Collectively Moving Active Matter.” Institute of Science and Technology Austria, 2023. https://doi.org/10.15479/14530. ieee: M. Riedl, “Synchronization in collectively moving active matter,” Institute of Science and Technology Austria, 2023. ista: Riedl M. 2023. Synchronization in collectively moving active matter. Institute of Science and Technology Austria. mla: Riedl, Michael. Synchronization in Collectively Moving Active Matter. Institute of Science and Technology Austria, 2023, doi:10.15479/14530. short: M. Riedl, Synchronization in Collectively Moving Active Matter, Institute of Science and Technology Austria, 2023. date_created: 2023-11-15T09:59:03Z date_published: 2023-11-16T00:00:00Z date_updated: 2023-11-30T10:55:13Z day: '16' ddc: - '530' - '570' degree_awarded: PhD department: - _id: GradSch - _id: MiSi doi: 10.15479/14530 file: - access_level: open_access checksum: 52e1d0ab6c1abe59c82dfe8c9ff5f83a content_type: application/pdf creator: mriedl date_created: 2023-11-15T09:52:54Z date_updated: 2023-11-15T09:52:54Z file_id: '14536' file_name: Thesis_Riedl_2023_corr.pdf file_size: 36743942 relation: main_file success: 1 file_date_updated: 2023-11-15T09:52:54Z has_accepted_license: '1' keyword: - Synchronization - Collective Movement - Active Matter - Cell Migration - Active Colloids language: - iso: eng month: '11' oa: 1 oa_version: Updated Version page: '260' publication_identifier: issn: - 2663 - 337X publication_status: published publisher: Institute of Science and Technology Austria related_material: record: - id: '10703' relation: part_of_dissertation status: public - id: '10791' relation: part_of_dissertation status: public - id: '7932' relation: part_of_dissertation status: public - id: '461' relation: part_of_dissertation status: public - id: '12726' relation: old_edition status: public status: public supervisor: - first_name: Björn full_name: Hof, Björn id: 3A374330-F248-11E8-B48F-1D18A9856A87 last_name: Hof orcid: 0000-0003-2057-2754 title: Synchronization in collectively moving active matter type: dissertation user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9 year: '2023' ... --- _id: '14361' abstract: - lang: eng text: Whether one considers swarming insects, flocking birds, or bacterial colonies, collective motion arises from the coordination of individuals and entails the adjustment of their respective velocities. In particular, in close confinements, such as those encountered by dense cell populations during development or regeneration, collective migration can only arise coordinately. Yet, how individuals unify their velocities is often not understood. Focusing on a finite number of cells in circular confinements, we identify waves of polymerizing actin that function as a pacemaker governing the speed of individual cells. We show that the onset of collective motion coincides with the synchronization of the wave nucleation frequencies across the population. Employing a simpler and more readily accessible mechanical model system of active spheres, we identify the synchronization of the individuals’ internal oscillators as one of the essential requirements to reach the corresponding collective state. The mechanical ‘toy’ experiment illustrates that the global synchronous state is achieved by nearest neighbor coupling. We suggest by analogy that local coupling and the synchronization of actin waves are essential for the emergent, self-organized motion of cell collectives. acknowledged_ssus: - _id: Bio - _id: LifeSc - _id: M-Shop acknowledgement: We thank K. O’Keeffe, E. Hannezo, P. Devreotes, C. Dessalles, and E. Martens for discussion and/or critical reading of the manuscript; the Bioimaging Facility of ISTA for excellent support, as well as the Life Science Facility and the Miba Machine Shop of ISTA. This work was supported by the European Research Council (ERC StG 281556 and CoG 724373) to M.S. article_number: '5633' article_processing_charge: Yes article_type: original author: - first_name: Michael full_name: Riedl, Michael id: 3BE60946-F248-11E8-B48F-1D18A9856A87 last_name: Riedl orcid: 0000-0003-4844-6311 - first_name: Isabelle D full_name: Mayer, Isabelle D id: 61763940-15b2-11ec-abd3-cfaddfbc66b4 last_name: Mayer - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Björn full_name: Hof, Björn id: 3A374330-F248-11E8-B48F-1D18A9856A87 last_name: Hof orcid: 0000-0003-2057-2754 citation: ama: Riedl M, Mayer ID, Merrin J, Sixt MK, Hof B. Synchronization in collectively moving inanimate and living active matter. Nature Communications. 2023;14. doi:10.1038/s41467-023-41432-1 apa: Riedl, M., Mayer, I. D., Merrin, J., Sixt, M. K., & Hof, B. (2023). Synchronization in collectively moving inanimate and living active matter. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-023-41432-1 chicago: Riedl, Michael, Isabelle D Mayer, Jack Merrin, Michael K Sixt, and Björn Hof. “Synchronization in Collectively Moving Inanimate and Living Active Matter.” Nature Communications. Springer Nature, 2023. https://doi.org/10.1038/s41467-023-41432-1. ieee: M. Riedl, I. D. Mayer, J. Merrin, M. K. Sixt, and B. Hof, “Synchronization in collectively moving inanimate and living active matter,” Nature Communications, vol. 14. Springer Nature, 2023. ista: Riedl M, Mayer ID, Merrin J, Sixt MK, Hof B. 2023. Synchronization in collectively moving inanimate and living active matter. Nature Communications. 14, 5633. mla: Riedl, Michael, et al. “Synchronization in Collectively Moving Inanimate and Living Active Matter.” Nature Communications, vol. 14, 5633, Springer Nature, 2023, doi:10.1038/s41467-023-41432-1. short: M. Riedl, I.D. Mayer, J. Merrin, M.K. Sixt, B. Hof, Nature Communications 14 (2023). date_created: 2023-09-24T22:01:10Z date_published: 2023-09-13T00:00:00Z date_updated: 2023-12-13T12:29:41Z day: '13' ddc: - '530' - '570' department: - _id: MiSi - _id: NanoFab - _id: BjHo doi: 10.1038/s41467-023-41432-1 ec_funded: 1 external_id: isi: - '001087583700030' pmid: - '37704595' file: - access_level: open_access checksum: 82d2d4ad736cc8493db8ce45cd313f7b content_type: application/pdf creator: dernst date_created: 2023-09-25T08:32:37Z date_updated: 2023-09-25T08:32:37Z file_id: '14366' file_name: 2023_NatureComm_Riedl.pdf file_size: 2317272 relation: main_file success: 1 file_date_updated: 2023-09-25T08:32:37Z has_accepted_license: '1' intvolume: ' 14' isi: 1 language: - iso: eng month: '09' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: Nature Communications publication_identifier: eissn: - 2041-1723 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Synchronization in collectively moving inanimate and living active matter tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 14 year: '2023' ... --- _id: '14360' abstract: - lang: eng text: To navigate through diverse tissues, migrating cells must balance persistent self-propelled motion with adaptive behaviors to circumvent obstacles. We identify a curvature-sensing mechanism underlying obstacle evasion in immune-like cells. Specifically, we propose that actin polymerization at the advancing edge of migrating cells is inhibited by the curvature-sensitive BAR domain protein Snx33 in regions with inward plasma membrane curvature. The genetic perturbation of this machinery reduces the cells’ capacity to evade obstructions combined with faster and more persistent cell migration in obstacle-free environments. Our results show how cells can read out their surface topography and utilize actin and plasma membrane biophysics to interpret their environment, allowing them to adaptively decide if they should move ahead or turn away. On the basis of our findings, we propose that the natural diversity of BAR domain proteins may allow cells to tune their curvature sensing machinery to match the shape characteristics in their environment. acknowledgement: "We thank Jan Ellenberg, Leanne Strauss, Anusha Gopalan, and Jia Hui Li for critical feedback on the manuscript and the Life Science Editors for editing assistance. The plasmid with hSnx33 was a kind gift from Duanqing Pei. Cell line with GFP-tagged IRSp53 was a kind gift from Orion Weiner. We thank Brian Graziano for providing protocols, reagents, and key advice to generate CRISPR knockout HL-60 cells. We thank the EMBL flow cytometry core facility, the EMBL advanced light microscopy facility, the EMBL proteomics facility, and the EMBL genomics core facility for support and advice. We thank Anusha Gopalan and Martin Bergert for their support during mechanical measurements by AFM. We thank Estela Sosa Osorio for technical assistance for the co-immunoprecipitation. We thank the EMBL genome biology computational support (and specially Charles Girardot and Jelle Scholtalbers) for critical assistance during RNAseq analysis. We thank Hans Kristian Hannibal‐Bach for his technical assistance during the lipidomic analysis of plasma membrane isolates. We thank Steffen Burgold for their support with LLS7 microscope in the ZEISS Microscopy Customer Center Europe. We acknowledge the financial support of the European Molecular Biology Laboratory (EMBL) to A.D.-M., Y.S., A.K., and A.E., the EMBL Interdisciplinary Postdocs (EIPOD) program under Marie Sklodowska-Curie COFUND actions MSCA-COFUND-FP to M.S.B. and M. S. (grant agreement number: 847543), the BEST program funding by FCT (SFRH/BEST/150300/2019) to S.D.A. and the Joachim Herz Stiftung Add-on Fellowship for Interdisciplinary Science to E.S.\r\nOpen Access funding enabled and organized by Projekt DEAL." article_number: '5644' article_processing_charge: Yes (via OA deal) article_type: original author: - first_name: Ewa full_name: Sitarska, Ewa last_name: Sitarska - first_name: Silvia Dias full_name: Almeida, Silvia Dias last_name: Almeida - first_name: Marianne Sandvold full_name: Beckwith, Marianne Sandvold last_name: Beckwith - first_name: Julian A full_name: Stopp, Julian A id: 489E3F00-F248-11E8-B48F-1D18A9856A87 last_name: Stopp - first_name: Jakub full_name: Czuchnowski, Jakub last_name: Czuchnowski - first_name: Marc full_name: Siggel, Marc last_name: Siggel - first_name: Rita full_name: Roessner, Rita last_name: Roessner - first_name: Aline full_name: Tschanz, Aline last_name: Tschanz - first_name: Christer full_name: Ejsing, Christer last_name: Ejsing - first_name: Yannick full_name: Schwab, Yannick last_name: Schwab - first_name: Jan full_name: Kosinski, Jan last_name: Kosinski - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Anna full_name: Kreshuk, Anna last_name: Kreshuk - first_name: Anna full_name: Erzberger, Anna last_name: Erzberger - first_name: Alba full_name: Diz-Muñoz, Alba last_name: Diz-Muñoz citation: ama: Sitarska E, Almeida SD, Beckwith MS, et al. Sensing their plasma membrane curvature allows migrating cells to circumvent obstacles. Nature Communications. 2023;14. doi:10.1038/s41467-023-41173-1 apa: Sitarska, E., Almeida, S. D., Beckwith, M. S., Stopp, J. A., Czuchnowski, J., Siggel, M., … Diz-Muñoz, A. (2023). Sensing their plasma membrane curvature allows migrating cells to circumvent obstacles. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-023-41173-1 chicago: Sitarska, Ewa, Silvia Dias Almeida, Marianne Sandvold Beckwith, Julian A Stopp, Jakub Czuchnowski, Marc Siggel, Rita Roessner, et al. “Sensing Their Plasma Membrane Curvature Allows Migrating Cells to Circumvent Obstacles.” Nature Communications. Springer Nature, 2023. https://doi.org/10.1038/s41467-023-41173-1. ieee: E. Sitarska et al., “Sensing their plasma membrane curvature allows migrating cells to circumvent obstacles,” Nature Communications, vol. 14. Springer Nature, 2023. ista: Sitarska E, Almeida SD, Beckwith MS, Stopp JA, Czuchnowski J, Siggel M, Roessner R, Tschanz A, Ejsing C, Schwab Y, Kosinski J, Sixt MK, Kreshuk A, Erzberger A, Diz-Muñoz A. 2023. Sensing their plasma membrane curvature allows migrating cells to circumvent obstacles. Nature Communications. 14, 5644. mla: Sitarska, Ewa, et al. “Sensing Their Plasma Membrane Curvature Allows Migrating Cells to Circumvent Obstacles.” Nature Communications, vol. 14, 5644, Springer Nature, 2023, doi:10.1038/s41467-023-41173-1. short: E. Sitarska, S.D. Almeida, M.S. Beckwith, J.A. Stopp, J. Czuchnowski, M. Siggel, R. Roessner, A. Tschanz, C. Ejsing, Y. Schwab, J. Kosinski, M.K. Sixt, A. Kreshuk, A. Erzberger, A. Diz-Muñoz, Nature Communications 14 (2023). date_created: 2023-09-24T22:01:10Z date_published: 2023-09-13T00:00:00Z date_updated: 2023-12-21T14:30:01Z day: '13' ddc: - '570' department: - _id: MiSi doi: 10.1038/s41467-023-41173-1 external_id: isi: - '001087583700008' pmid: - '37704612' file: - access_level: open_access checksum: ad670e3b3c64fc585675948370f6b149 content_type: application/pdf creator: dernst date_created: 2023-09-25T08:22:58Z date_updated: 2023-09-25T08:22:58Z file_id: '14365' file_name: 2023_NatureComm_Sitarska.pdf file_size: 2725421 relation: main_file success: 1 file_date_updated: 2023-09-25T08:22:58Z has_accepted_license: '1' intvolume: ' 14' isi: 1 language: - iso: eng month: '09' oa: 1 oa_version: Published Version pmid: 1 publication: Nature Communications publication_identifier: eissn: - 2041-1723 publication_status: published publisher: Springer Nature quality_controlled: '1' related_material: record: - id: '14697' relation: dissertation_contains status: public scopus_import: '1' status: public title: Sensing their plasma membrane curvature allows migrating cells to circumvent obstacles tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 14 year: '2023' ... --- _id: '14274' abstract: - lang: eng text: Immune responses rely on the rapid and coordinated migration of leukocytes. Whereas it is well established that single-cell migration is often guided by gradients of chemokines and other chemoattractants, it remains poorly understood how these gradients are generated, maintained, and modulated. By combining experimental data with theory on leukocyte chemotaxis guided by the G protein–coupled receptor (GPCR) CCR7, we demonstrate that in addition to its role as the sensory receptor that steers migration, CCR7 also acts as a generator and a modulator of chemotactic gradients. Upon exposure to the CCR7 ligand CCL19, dendritic cells (DCs) effectively internalize the receptor and ligand as part of the canonical GPCR desensitization response. We show that CCR7 internalization also acts as an effective sink for the chemoattractant, dynamically shaping the spatiotemporal distribution of the chemokine. This mechanism drives complex collective migration patterns, enabling DCs to create or sharpen chemotactic gradients. We further show that these self-generated gradients can sustain the long-range guidance of DCs, adapt collective migration patterns to the size and geometry of the environment, and provide a guidance cue for other comigrating cells. Such a dual role of CCR7 as a GPCR that both senses and consumes its ligand can thus provide a novel mode of cellular self-organization. acknowledgement: "We thank I. de Vries and the Scientific Service Units (Life Sciences, Bioimaging, Nanofabrication, Preclinical and Miba Machine Shop) of the Institute of Science and Technology Austria for excellent support, as well as all the rotation students assisting in the laboratory work (B. Zens, H. Schön, and D. Babic).\r\nThis work was supported by grants from the European Research Council under the European Union’s Horizon 2020 research to M.S. (grant agreement no. 724373) and to E.H. (grant agreement no. 851288), and a grant by the Austrian Science Fund (DK Nanocell W1250-B20) to M.S. J.A. was supported by the Jenny and Antti Wihuri Foundation and Research Council of Finland's Flagship Programme InFLAMES (decision number: 357910). M.C.U. was supported by the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 754411." article_number: adc9584 article_processing_charge: No article_type: original author: - first_name: Jonna H full_name: Alanko, Jonna H id: 2CC12E8C-F248-11E8-B48F-1D18A9856A87 last_name: Alanko orcid: 0000-0002-7698-3061 - first_name: Mehmet C full_name: Ucar, Mehmet C id: 50B2A802-6007-11E9-A42B-EB23E6697425 last_name: Ucar orcid: 0000-0003-0506-4217 - first_name: Nikola full_name: Canigova, Nikola id: 3795523E-F248-11E8-B48F-1D18A9856A87 last_name: Canigova orcid: 0000-0002-8518-5926 - first_name: Julian A full_name: Stopp, Julian A id: 489E3F00-F248-11E8-B48F-1D18A9856A87 last_name: Stopp - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Edouard B full_name: Hannezo, Edouard B id: 3A9DB764-F248-11E8-B48F-1D18A9856A87 last_name: Hannezo orcid: 0000-0001-6005-1561 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Alanko JH, Ucar MC, Canigova N, et al. CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective leukocyte migration. Science Immunology. 2023;8(87). doi:10.1126/sciimmunol.adc9584 apa: Alanko, J. H., Ucar, M. C., Canigova, N., Stopp, J. A., Schwarz, J., Merrin, J., … Sixt, M. K. (2023). CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective leukocyte migration. Science Immunology. American Association for the Advancement of Science. https://doi.org/10.1126/sciimmunol.adc9584 chicago: Alanko, Jonna H, Mehmet C Ucar, Nikola Canigova, Julian A Stopp, Jan Schwarz, Jack Merrin, Edouard B Hannezo, and Michael K Sixt. “CCR7 Acts as Both a Sensor and a Sink for CCL19 to Coordinate Collective Leukocyte Migration.” Science Immunology. American Association for the Advancement of Science, 2023. https://doi.org/10.1126/sciimmunol.adc9584. ieee: J. H. Alanko et al., “CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective leukocyte migration,” Science Immunology, vol. 8, no. 87. American Association for the Advancement of Science, 2023. ista: Alanko JH, Ucar MC, Canigova N, Stopp JA, Schwarz J, Merrin J, Hannezo EB, Sixt MK. 2023. CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective leukocyte migration. Science Immunology. 8(87), adc9584. mla: Alanko, Jonna H., et al. “CCR7 Acts as Both a Sensor and a Sink for CCL19 to Coordinate Collective Leukocyte Migration.” Science Immunology, vol. 8, no. 87, adc9584, American Association for the Advancement of Science, 2023, doi:10.1126/sciimmunol.adc9584. short: J.H. Alanko, M.C. Ucar, N. Canigova, J.A. Stopp, J. Schwarz, J. Merrin, E.B. Hannezo, M.K. Sixt, Science Immunology 8 (2023). date_created: 2023-09-06T08:07:51Z date_published: 2023-09-01T00:00:00Z date_updated: 2023-12-21T14:30:01Z day: '01' department: - _id: MiSi - _id: EdHa - _id: NanoFab doi: 10.1126/sciimmunol.adc9584 ec_funded: 1 external_id: isi: - '001062110600003' pmid: - '37656776' intvolume: ' 8' isi: 1 issue: '87' keyword: - General Medicine - Immunology language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1126/sciimmunol.adc9584 month: '09' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 05943252-7A3F-11EA-A408-12923DDC885E call_identifier: H2020 grant_number: '851288' name: Design Principles of Branching Morphogenesis - _id: 265E2996-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: W01250-B20 name: Nano-Analytics of Cellular Systems - _id: 260C2330-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '754411' name: ISTplus - Postdoctoral Fellowships publication: Science Immunology publication_identifier: issn: - 2470-9468 publication_status: published publisher: American Association for the Advancement of Science quality_controlled: '1' related_material: record: - id: '14279' relation: research_data status: public - id: '14697' relation: dissertation_contains status: public scopus_import: '1' status: public title: CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective leukocyte migration type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2023' ... --- _id: '14697' acknowledged_ssus: - _id: LifeSc - _id: Bio alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Julian A full_name: Stopp, Julian A id: 489E3F00-F248-11E8-B48F-1D18A9856A87 last_name: Stopp citation: ama: 'Stopp JA. Neutrophils on the hunt: Migratory strategies employed by neutrophils to fulfill their effector function. 2023. doi:10.15479/at:ista:14697' apa: 'Stopp, J. A. (2023). Neutrophils on the hunt: Migratory strategies employed by neutrophils to fulfill their effector function. Institute of Science and Technology Austria. https://doi.org/10.15479/at:ista:14697' chicago: 'Stopp, Julian A. “Neutrophils on the Hunt: Migratory Strategies Employed by Neutrophils to Fulfill Their Effector Function.” Institute of Science and Technology Austria, 2023. https://doi.org/10.15479/at:ista:14697.' ieee: 'J. A. Stopp, “Neutrophils on the hunt: Migratory strategies employed by neutrophils to fulfill their effector function,” Institute of Science and Technology Austria, 2023.' ista: 'Stopp JA. 2023. Neutrophils on the hunt: Migratory strategies employed by neutrophils to fulfill their effector function. Institute of Science and Technology Austria.' mla: 'Stopp, Julian A. Neutrophils on the Hunt: Migratory Strategies Employed by Neutrophils to Fulfill Their Effector Function. Institute of Science and Technology Austria, 2023, doi:10.15479/at:ista:14697.' short: 'J.A. Stopp, Neutrophils on the Hunt: Migratory Strategies Employed by Neutrophils to Fulfill Their Effector Function, Institute of Science and Technology Austria, 2023.' date_created: 2023-12-18T19:14:28Z date_published: 2023-12-20T00:00:00Z date_updated: 2023-12-21T14:30:02Z day: '20' ddc: - '570' degree_awarded: PhD department: - _id: GradSch - _id: MiSi doi: 10.15479/at:ista:14697 ec_funded: 1 file: - access_level: closed checksum: 457927165d5d556305d3086f6b83e5c7 content_type: application/pdf creator: jstopp date_created: 2023-12-20T09:35:34Z date_updated: 2023-12-20T09:35:34Z embargo: 2024-12-20 embargo_to: open_access file_id: '14699' file_name: Thesis.pdf file_size: 51585778 relation: main_file - access_level: closed checksum: e8d26449ac461f5e8478a62c9507506f content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document creator: jstopp date_created: 2023-12-20T09:35:35Z date_updated: 2023-12-20T10:41:42Z file_id: '14700' file_name: Thesis.docx file_size: 69625950 relation: source_file file_date_updated: 2023-12-20T10:41:42Z has_accepted_license: '1' language: - iso: eng month: '12' oa_version: Published Version page: '226' project: - _id: 2564DBCA-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '665385' name: International IST Doctoral Program publication_identifier: isbn: - 978-3-99078-038-1 issn: - 2663 - 337X publication_status: published publisher: Institute of Science and Technology Austria related_material: record: - id: '6328' relation: part_of_dissertation status: public - id: '7885' relation: part_of_dissertation status: public - id: '12272' relation: part_of_dissertation status: public - id: '14274' relation: part_of_dissertation status: public - id: '14360' relation: part_of_dissertation status: public status: public supervisor: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 title: 'Neutrophils on the hunt: Migratory strategies employed by neutrophils to fulfill their effector function' type: dissertation user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9 year: '2023' ... --- _id: '14848' abstract: - lang: eng text: Regulating protein states is considered the core function of chaperones. However, despite their importance to all major cellular processes, the conformational changes that chaperones impart on polypeptide chains are difficult to study directly due to their heterogeneous, dynamic, and multi-step nature. Here, we review recent advances towards this aim using single-molecule manipulation methods, which are rapidly revealing new mechanisms of conformational control and helping to define a different perspective on the chaperone function. alternative_title: - New Developments in NMR article_processing_charge: No author: - first_name: F. full_name: Wruck, F. last_name: Wruck - first_name: Mario full_name: Avellaneda Sarrió, Mario id: DC4BA84C-56E6-11EA-AD5D-348C3DDC885E last_name: Avellaneda Sarrió orcid: 0000-0001-6406-524X - first_name: M. M. full_name: Naqvi, M. M. last_name: Naqvi - first_name: E. J. full_name: Koers, E. J. last_name: Koers - first_name: K. full_name: Till, K. last_name: Till - first_name: L. full_name: Gross, L. last_name: Gross - first_name: F. full_name: Moayed, F. last_name: Moayed - first_name: A. full_name: Roland, A. last_name: Roland - first_name: L. W. H. J. full_name: Heling, L. W. H. J. last_name: Heling - first_name: A. full_name: Mashaghi, A. last_name: Mashaghi - first_name: S. J. full_name: Tans, S. J. last_name: Tans citation: ama: 'Wruck F, Avellaneda Sarrió M, Naqvi MM, et al. Probing Single Chaperone Substrates. In: Hiller S, Liu M, He L, eds. Biophysics of Molecular Chaperones. Vol 29. Royal Society of Chemistry; 2023:278-318. doi:10.1039/bk9781839165986-00278' apa: Wruck, F., Avellaneda Sarrió, M., Naqvi, M. M., Koers, E. J., Till, K., Gross, L., … Tans, S. J. (2023). Probing Single Chaperone Substrates. In S. Hiller, M. Liu, & L. He (Eds.), Biophysics of Molecular Chaperones (Vol. 29, pp. 278–318). Royal Society of Chemistry. https://doi.org/10.1039/bk9781839165986-00278 chicago: Wruck, F., Mario Avellaneda Sarrió, M. M. Naqvi, E. J. Koers, K. Till, L. Gross, F. Moayed, et al. “Probing Single Chaperone Substrates.” In Biophysics of Molecular Chaperones, edited by Sebastian Hiller, Maili Liu, and Lichun He, 29:278–318. Royal Society of Chemistry, 2023. https://doi.org/10.1039/bk9781839165986-00278. ieee: F. Wruck et al., “Probing Single Chaperone Substrates,” in Biophysics of Molecular Chaperones, vol. 29, S. Hiller, M. Liu, and L. He, Eds. Royal Society of Chemistry, 2023, pp. 278–318. ista: 'Wruck F, Avellaneda Sarrió M, Naqvi MM, Koers EJ, Till K, Gross L, Moayed F, Roland A, Heling LWHJ, Mashaghi A, Tans SJ. 2023.Probing Single Chaperone Substrates. In: Biophysics of Molecular Chaperones. New Developments in NMR, vol. 29, 278–318.' mla: Wruck, F., et al. “Probing Single Chaperone Substrates.” Biophysics of Molecular Chaperones, edited by Sebastian Hiller et al., vol. 29, Royal Society of Chemistry, 2023, pp. 278–318, doi:10.1039/bk9781839165986-00278. short: F. Wruck, M. Avellaneda Sarrió, M.M. Naqvi, E.J. Koers, K. Till, L. Gross, F. Moayed, A. Roland, L.W.H.J. Heling, A. Mashaghi, S.J. Tans, in:, S. Hiller, M. Liu, L. He (Eds.), Biophysics of Molecular Chaperones, Royal Society of Chemistry, 2023, pp. 278–318. date_created: 2024-01-22T08:07:02Z date_published: 2023-11-01T00:00:00Z date_updated: 2024-01-23T12:01:53Z day: '01' department: - _id: MiSi doi: 10.1039/bk9781839165986-00278 editor: - first_name: Sebastian full_name: Hiller, Sebastian last_name: Hiller - first_name: Maili full_name: Liu, Maili last_name: Liu - first_name: Lichun full_name: He, Lichun last_name: He intvolume: ' 29' language: - iso: eng month: '11' oa_version: None page: 278-318 publication: Biophysics of Molecular Chaperones publication_identifier: eisbn: - '9781839165993' isbn: - '9781839162824' publication_status: published publisher: Royal Society of Chemistry quality_controlled: '1' status: public title: Probing Single Chaperone Substrates type: book_chapter user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 29 year: '2023' ... --- _id: '9794' abstract: - lang: eng text: 'Lymph nodes (LNs) comprise two main structural elements: fibroblastic reticular cells that form dedicated niches for immune cell interaction and capsular fibroblasts that build a shell around the organ. Immunological challenge causes LNs to increase more than tenfold in size within a few days. Here, we characterized the biomechanics of LN swelling on the cellular and organ scale. We identified lymphocyte trapping by influx and proliferation as drivers of an outward pressure force, causing fibroblastic reticular cells of the T-zone (TRCs) and their associated conduits to stretch. After an initial phase of relaxation, TRCs sensed the resulting strain through cell matrix adhesions, which coordinated local growth and remodeling of the stromal network. While the expanded TRC network readopted its typical configuration, a massive fibrotic reaction of the organ capsule set in and countered further organ expansion. Thus, different fibroblast populations mechanically control LN swelling in a multitier fashion.' acknowledged_ssus: - _id: Bio - _id: EM-Fac - _id: PreCl - _id: LifeSc acknowledgement: This research was supported by the Scientific Service Units of IST Austria through resources provided by the Imaging and Optics, Electron Microscopy, Preclinical and Life Science Facilities. We thank C. Moussion for providing anti-PNAd antibody and D. Critchley for Talin1-floxed mice, and E. Papusheva for providing a custom 3D channel alignment script. This work was supported by a European Research Council grant ERC-CoG-72437 to M.S. M.H. was supported by Czech Sciencundation GACR 20-24603Y and Charles University PRIMUS/20/MED/013. article_processing_charge: No article_type: original author: - first_name: Frank P full_name: Assen, Frank P id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87 last_name: Assen orcid: 0000-0003-3470-6119 - first_name: Jun full_name: Abe, Jun last_name: Abe - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Shayan full_name: Shamipour, Shayan id: 40B34FE2-F248-11E8-B48F-1D18A9856A87 last_name: Shamipour - first_name: Walter full_name: Kaufmann, Walter id: 3F99E422-F248-11E8-B48F-1D18A9856A87 last_name: Kaufmann orcid: 0000-0001-9735-5315 - first_name: Tommaso full_name: Costanzo, Tommaso id: D93824F4-D9BA-11E9-BB12-F207E6697425 last_name: Costanzo orcid: 0000-0001-9732-3815 - first_name: Gabriel full_name: Krens, Gabriel id: 2B819732-F248-11E8-B48F-1D18A9856A87 last_name: Krens orcid: 0000-0003-4761-5996 - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Burkhard full_name: Ludewig, Burkhard last_name: Ludewig - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 - first_name: Wolfgang full_name: Weninger, Wolfgang last_name: Weninger - first_name: Edouard B full_name: Hannezo, Edouard B id: 3A9DB764-F248-11E8-B48F-1D18A9856A87 last_name: Hannezo orcid: 0000-0001-6005-1561 - first_name: Sanjiv A. full_name: Luther, Sanjiv A. last_name: Luther - first_name: Jens V. full_name: Stein, Jens V. last_name: Stein - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-4561-241X citation: ama: Assen FP, Abe J, Hons M, et al. Multitier mechanics control stromal adaptations in swelling lymph nodes. Nature Immunology. 2022;23:1246-1255. doi:10.1038/s41590-022-01257-4 apa: Assen, F. P., Abe, J., Hons, M., Hauschild, R., Shamipour, S., Kaufmann, W., … Sixt, M. K. (2022). Multitier mechanics control stromal adaptations in swelling lymph nodes. Nature Immunology. Springer Nature. https://doi.org/10.1038/s41590-022-01257-4 chicago: Assen, Frank P, Jun Abe, Miroslav Hons, Robert Hauschild, Shayan Shamipour, Walter Kaufmann, Tommaso Costanzo, et al. “Multitier Mechanics Control Stromal Adaptations in Swelling Lymph Nodes.” Nature Immunology. Springer Nature, 2022. https://doi.org/10.1038/s41590-022-01257-4. ieee: F. P. Assen et al., “Multitier mechanics control stromal adaptations in swelling lymph nodes,” Nature Immunology, vol. 23. Springer Nature, pp. 1246–1255, 2022. ista: Assen FP, Abe J, Hons M, Hauschild R, Shamipour S, Kaufmann W, Costanzo T, Krens G, Brown M, Ludewig B, Hippenmeyer S, Heisenberg C-PJ, Weninger W, Hannezo EB, Luther SA, Stein JV, Sixt MK. 2022. Multitier mechanics control stromal adaptations in swelling lymph nodes. Nature Immunology. 23, 1246–1255. mla: Assen, Frank P., et al. “Multitier Mechanics Control Stromal Adaptations in Swelling Lymph Nodes.” Nature Immunology, vol. 23, Springer Nature, 2022, pp. 1246–55, doi:10.1038/s41590-022-01257-4. short: F.P. Assen, J. Abe, M. Hons, R. Hauschild, S. Shamipour, W. Kaufmann, T. Costanzo, G. Krens, M. Brown, B. Ludewig, S. Hippenmeyer, C.-P.J. Heisenberg, W. Weninger, E.B. Hannezo, S.A. Luther, J.V. Stein, M.K. Sixt, Nature Immunology 23 (2022) 1246–1255. date_created: 2021-08-06T09:09:11Z date_published: 2022-07-11T00:00:00Z date_updated: 2023-08-02T06:53:07Z day: '11' ddc: - '570' department: - _id: SiHi - _id: CaHe - _id: EdHa - _id: EM-Fac - _id: Bio - _id: MiSi doi: 10.1038/s41590-022-01257-4 ec_funded: 1 external_id: isi: - '000822975900002' file: - access_level: open_access checksum: 628e7b49809f22c75b428842efe70c68 content_type: application/pdf creator: dernst date_created: 2022-07-25T07:11:32Z date_updated: 2022-07-25T07:11:32Z file_id: '11642' file_name: 2022_NatureImmunology_Assen.pdf file_size: 11475325 relation: main_file success: 1 file_date_updated: 2022-07-25T07:11:32Z has_accepted_license: '1' intvolume: ' 23' isi: 1 language: - iso: eng month: '07' oa: 1 oa_version: Published Version page: 1246-1255 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: Nature Immunology publication_identifier: eissn: - 1529-2916 issn: - 1529-2908 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Multitier mechanics control stromal adaptations in swelling lymph nodes tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 23 year: '2022' ... --- _id: '11588' abstract: - lang: eng text: Visualizing cell behavior and effector function on a single cell level has been crucial for understanding key aspects of mammalian biology. Due to their small size, large number and rapid recruitment into thrombi, there is a lack of data on fate and behavior of individual platelets in thrombosis and hemostasis. Here we report the use of platelet lineage restricted multi-color reporter mouse strains to delineate platelet function on a single cell level. We show that genetic labeling allows for single platelet and megakaryocyte (MK) tracking and morphological analysis in vivo and in vitro, while not affecting lineage functions. Using Cre-driven Confetti expression, we provide insights into temporal gene expression patterns as well as spatial clustering of MK in the bone marrow. In the vasculature, shape analysis of activated platelets recruited to thrombi identifies ubiquitous filopodia formation with no evidence of lamellipodia formation. Single cell tracking in complex thrombi reveals prominent myosin-dependent motility of platelets and highlights thrombus formation as a highly dynamic process amenable to modification and intervention of the acto-myosin cytoskeleton. Platelet function assays combining flow cytrometry, as well as in vivo, ex vivo and in vitro imaging show unaltered platelet functions of multicolor reporter mice compared to wild-type controls. In conclusion, platelet lineage multicolor reporter mice prove useful in furthering our understanding of platelet and MK biology on a single cell level. acknowledgement: "This study was supported by the Deutsche Forschungsgemeinschaft (DFG) SFB 914 ( to SM [B02 and Z01]), the DFG SFB 1123 (to SM [B06]), the DFG FOR 2033 (to SM), the German\r\nCenter for Cardiovascular Research (DZHK) (Clinician Scientist Programme), MHA 1.4VD (to SM), Postdoc Start-up Grant, 81X3600213 (to FG), 81X3600222 (to LN), the FP7 program\r\n(project 260309, PRESTIGE [to SM]). This project has received funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement No. 83344, ERC-2018-ADG “IMMUNOTHROMBOSIS” [to SM] and the Marie Skłodowska Curie Individual Fellowship (EU project 747687, LamelliActin [to FG]). " article_processing_charge: No article_type: original author: - first_name: Leo full_name: Nicolai, Leo last_name: Nicolai - first_name: Rainer full_name: Kaiser, Rainer last_name: Kaiser - first_name: Raphael full_name: Escaig, Raphael last_name: Escaig - first_name: Marie Louise full_name: Hoffknecht, Marie Louise last_name: Hoffknecht - first_name: Afra full_name: Anjum, Afra last_name: Anjum - first_name: Alexander full_name: Leunig, Alexander last_name: Leunig - first_name: Joachim full_name: Pircher, Joachim last_name: Pircher - first_name: Andreas full_name: Ehrlich, Andreas last_name: Ehrlich - first_name: Michael full_name: Lorenz, Michael last_name: Lorenz - first_name: Hellen full_name: Ishikawa-Ankerhold, Hellen last_name: Ishikawa-Ankerhold - first_name: William C. full_name: Aird, William C. last_name: Aird - first_name: Steffen full_name: Massberg, Steffen last_name: Massberg - first_name: Florian R full_name: Gärtner, Florian R id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 citation: ama: Nicolai L, Kaiser R, Escaig R, et al. Single platelet and megakaryocyte morpho-dynamics uncovered by multicolor reporter mouse strains in vitro and in vivo. Haematologica. 2022;107(7):1669-1680. doi:10.3324/haematol.2021.278896 apa: Nicolai, L., Kaiser, R., Escaig, R., Hoffknecht, M. L., Anjum, A., Leunig, A., … Gärtner, F. R. (2022). Single platelet and megakaryocyte morpho-dynamics uncovered by multicolor reporter mouse strains in vitro and in vivo. Haematologica. Ferrata Storti Foundation. https://doi.org/10.3324/haematol.2021.278896 chicago: Nicolai, Leo, Rainer Kaiser, Raphael Escaig, Marie Louise Hoffknecht, Afra Anjum, Alexander Leunig, Joachim Pircher, et al. “Single Platelet and Megakaryocyte Morpho-Dynamics Uncovered by Multicolor Reporter Mouse Strains in Vitro and in Vivo.” Haematologica. Ferrata Storti Foundation, 2022. https://doi.org/10.3324/haematol.2021.278896. ieee: L. Nicolai et al., “Single platelet and megakaryocyte morpho-dynamics uncovered by multicolor reporter mouse strains in vitro and in vivo,” Haematologica, vol. 107, no. 7. Ferrata Storti Foundation, pp. 1669–1680, 2022. ista: Nicolai L, Kaiser R, Escaig R, Hoffknecht ML, Anjum A, Leunig A, Pircher J, Ehrlich A, Lorenz M, Ishikawa-Ankerhold H, Aird WC, Massberg S, Gärtner FR. 2022. Single platelet and megakaryocyte morpho-dynamics uncovered by multicolor reporter mouse strains in vitro and in vivo. Haematologica. 107(7), 1669–1680. mla: Nicolai, Leo, et al. “Single Platelet and Megakaryocyte Morpho-Dynamics Uncovered by Multicolor Reporter Mouse Strains in Vitro and in Vivo.” Haematologica, vol. 107, no. 7, Ferrata Storti Foundation, 2022, pp. 1669–80, doi:10.3324/haematol.2021.278896. short: L. Nicolai, R. Kaiser, R. Escaig, M.L. Hoffknecht, A. Anjum, A. Leunig, J. Pircher, A. Ehrlich, M. Lorenz, H. Ishikawa-Ankerhold, W.C. Aird, S. Massberg, F.R. Gärtner, Haematologica 107 (2022) 1669–1680. date_created: 2022-07-17T22:01:54Z date_published: 2022-07-01T00:00:00Z date_updated: 2023-08-03T12:01:01Z day: '01' ddc: - '570' department: - _id: MiSi doi: 10.3324/haematol.2021.278896 ec_funded: 1 external_id: isi: - '000823746100018' file: - access_level: open_access checksum: 9b47830945f3c30428fe9cfee2dc4a8a content_type: application/pdf creator: dernst date_created: 2022-07-18T07:51:55Z date_updated: 2022-07-18T07:51:55Z file_id: '11595' file_name: 2022_Haematologica_Nicolai.pdf file_size: 1722094 relation: main_file success: 1 file_date_updated: 2022-07-18T07:51:55Z has_accepted_license: '1' intvolume: ' 107' isi: 1 issue: '7' language: - iso: eng license: https://creativecommons.org/licenses/by-nc/4.0/ month: '07' oa: 1 oa_version: Published Version page: 1669-1680 project: - _id: 260AA4E2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '747687' name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells publication: Haematologica publication_identifier: eissn: - 1592-8721 issn: - 0390-6078 publication_status: published publisher: Ferrata Storti Foundation quality_controlled: '1' scopus_import: '1' status: public title: Single platelet and megakaryocyte morpho-dynamics uncovered by multicolor reporter mouse strains in vitro and in vivo tmp: image: /images/cc_by_nc.png legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) short: CC BY-NC (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 107 year: '2022' ... --- _id: '11843' abstract: - lang: eng text: A key attribute of persistent or recurring bacterial infections is the ability of the pathogen to evade the host’s immune response. Many Enterobacteriaceae express type 1 pili, a pre-adapted virulence trait, to invade host epithelial cells and establish persistent infections. However, the molecular mechanisms and strategies by which bacteria actively circumvent the immune response of the host remain poorly understood. Here, we identified CD14, the major co-receptor for lipopolysaccharide detection, on mouse dendritic cells (DCs) as a binding partner of FimH, the protein located at the tip of the type 1 pilus of Escherichia coli. The FimH amino acids involved in CD14 binding are highly conserved across pathogenic and non-pathogenic strains. Binding of the pathogenic strain CFT073 to CD14 reduced DC migration by overactivation of integrins and blunted expression of co-stimulatory molecules by overactivating the NFAT (nuclear factor of activated T-cells) pathway, both rate-limiting factors of T cell activation. This response was binary at the single-cell level, but averaged in larger populations exposed to both piliated and non-piliated pathogens, presumably via the exchange of immunomodulatory cytokines. While defining an active molecular mechanism of immune evasion by pathogens, the interaction between FimH and CD14 represents a potential target to interfere with persistent and recurrent infections, such as urinary tract infections or Crohn’s disease. acknowledged_ssus: - _id: Bio - _id: PreCl - _id: EM-Fac acknowledgement: We thank Ulrich Dobrindt for providing UPEC strains CFT073, UTI89, and 536, Frank Assen, Vlad Gavra, Maximilian Götz, Bor Kavčič, Jonna Alanko, and Eva Kiermaier for help with experiments and Robert Hauschild, Julian Stopp, and Saren Tasciyan for help with data analysis. We thank the IST Austria Scientific Service Units, especially the Bioimaging facility, the Preclinical facility and the Electron microscopy facility for technical support, Jakob Wallner and all members of the Guet and Sixt lab for fruitful discussions and Daria Siekhaus for critically reading the manuscript. This work was supported by grants from the Austrian Research Promotion Agency (FEMtech 868984) to IG, the European Research Council (CoG 724373), and the Austrian Science Fund (FWF P29911) to MS. article_number: e78995 article_processing_charge: Yes article_type: original author: - first_name: Kathrin full_name: Tomasek, Kathrin id: 3AEC8556-F248-11E8-B48F-1D18A9856A87 last_name: Tomasek - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner - first_name: Ivana full_name: Glatzová, Ivana id: 727b3c7d-4939-11ec-89b3-b9b0750ab74d last_name: Glatzová - first_name: Michael S. full_name: Lukesch, Michael S. last_name: Lukesch - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. eLife. 2022;11. doi:10.7554/eLife.78995 apa: Tomasek, K., Leithner, A. F., Glatzová, I., Lukesch, M. S., Guet, C. C., & Sixt, M. K. (2022). Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.78995 chicago: Tomasek, Kathrin, Alexander F Leithner, Ivana Glatzová, Michael S. Lukesch, Calin C Guet, and Michael K Sixt. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack the Host Immune Response by Binding to CD14.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/eLife.78995. ieee: K. Tomasek, A. F. Leithner, I. Glatzová, M. S. Lukesch, C. C. Guet, and M. K. Sixt, “Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14,” eLife, vol. 11. eLife Sciences Publications, 2022. ista: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. 2022. Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. eLife. 11, e78995. mla: Tomasek, Kathrin, et al. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack the Host Immune Response by Binding to CD14.” ELife, vol. 11, e78995, eLife Sciences Publications, 2022, doi:10.7554/eLife.78995. short: K. Tomasek, A.F. Leithner, I. Glatzová, M.S. Lukesch, C.C. Guet, M.K. Sixt, ELife 11 (2022). date_created: 2022-08-14T22:01:46Z date_published: 2022-07-26T00:00:00Z date_updated: 2023-08-03T12:54:21Z day: '26' ddc: - '570' department: - _id: MiSi - _id: CaGu doi: 10.7554/eLife.78995 ec_funded: 1 external_id: isi: - '000838410200001' file: - access_level: open_access checksum: 002a3c7c7ea5caa9af9cfbea308f6ea4 content_type: application/pdf creator: cchlebak date_created: 2022-08-16T08:57:37Z date_updated: 2022-08-16T08:57:37Z file_id: '11861' file_name: 2022_eLife_Tomasek.pdf file_size: 2057577 relation: main_file success: 1 file_date_updated: 2022-08-16T08:57:37Z has_accepted_license: '1' intvolume: ' 11' isi: 1 language: - iso: eng month: '07' oa: 1 oa_version: Published Version project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 26018E70-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29911 name: Mechanical adaptation of lamellipodial actin publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' related_material: record: - id: '10316' relation: earlier_version status: public scopus_import: '1' status: public title: Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14 tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 11 year: '2022' ... --- _id: '12085' abstract: - lang: eng text: Molecular catch bonds are ubiquitous in biology and essential for processes like leucocyte extravasion1 and cellular mechanosensing2. Unlike normal (slip) bonds, catch bonds strengthen under tension. The current paradigm is that this feature provides ‘strength on demand3’, thus enabling cells to increase rigidity under stress1,4,5,6. However, catch bonds are often weaker than slip bonds because they have cryptic binding sites that are usually buried7,8. Here we show that catch bonds render reconstituted cytoskeletal actin networks stronger than slip bonds, even though the individual bonds are weaker. Simulations show that slip bonds remain trapped in stress-free areas, whereas weak binding allows catch bonds to mitigate crack initiation by moving to high-tension areas. This ‘dissociation on demand’ explains how cells combine mechanical strength with the adaptability required for shape change, and is relevant to diseases where catch bonding is compromised7,9, including focal segmental glomerulosclerosis10 caused by the α-actinin-4 mutant studied here. We surmise that catch bonds are the key to create life-like materials. acknowledgement: 'We thank M. van Hecke and C. Alkemade for critical reading of the manuscript. We thank P. R. ten Wolde, K. Storm, W. Ellenbroek, C. Broedersz, D. Brueckner and M. Berger for fruitful discussions. We thank W. Brieher and V. Tang from the University of Illinois for the kind gift of purified α-actinin-4 (WT and the K255E point mutant) and their plasmids; M. Kuit-Vinkenoog and J. den Haan for actin and further purification of α-actinin-4; A. Goutou and I. Isturiz-Petitjean for co-sedimentation measurements and V. Sunderlíková for the design, mutagenesis, cloning and purifying of the α-actinin-4 constructs used in the single-molecule experiments. We gratefully acknowledge financial support from the following sources: research program of the Netherlands Organization for Scientific Research (NWO) (S.J.T., A.R. and M.J.A.); ERC Starting Grant (335672-MINICELL) (G.H.K. and Y.M.). ‘BaSyC—Building a Synthetic Cell’ Gravitation grant (024.003.019) of the Netherlands Ministry of Education, Culture and Science (OCW) and the Netherlands Organisation for Scientific Research (G.H.K. and L.B.); and support from the National Institutes of Health (1R01GM126256) (T.K. and W.J.).' article_processing_charge: No article_type: original author: - first_name: Yuval full_name: Mulla, Yuval last_name: Mulla - first_name: Mario full_name: Avellaneda Sarrió, Mario id: DC4BA84C-56E6-11EA-AD5D-348C3DDC885E last_name: Avellaneda Sarrió orcid: 0000-0001-6406-524X - first_name: Antoine full_name: Roland, Antoine last_name: Roland - first_name: Lucia full_name: Baldauf, Lucia last_name: Baldauf - first_name: Wonyeong full_name: Jung, Wonyeong last_name: Jung - first_name: Taeyoon full_name: Kim, Taeyoon last_name: Kim - first_name: Sander J. full_name: Tans, Sander J. last_name: Tans - first_name: Gijsje H. full_name: Koenderink, Gijsje H. last_name: Koenderink citation: ama: Mulla Y, Avellaneda Sarrió M, Roland A, et al. Weak catch bonds make strong networks. Nature Materials. 2022;21(9):1019-1023. doi:10.1038/s41563-022-01288-0 apa: Mulla, Y., Avellaneda Sarrió, M., Roland, A., Baldauf, L., Jung, W., Kim, T., … Koenderink, G. H. (2022). Weak catch bonds make strong networks. Nature Materials. Springer Nature. https://doi.org/10.1038/s41563-022-01288-0 chicago: Mulla, Yuval, Mario Avellaneda Sarrió, Antoine Roland, Lucia Baldauf, Wonyeong Jung, Taeyoon Kim, Sander J. Tans, and Gijsje H. Koenderink. “Weak Catch Bonds Make Strong Networks.” Nature Materials. Springer Nature, 2022. https://doi.org/10.1038/s41563-022-01288-0. ieee: Y. Mulla et al., “Weak catch bonds make strong networks,” Nature Materials, vol. 21, no. 9. Springer Nature, pp. 1019–1023, 2022. ista: Mulla Y, Avellaneda Sarrió M, Roland A, Baldauf L, Jung W, Kim T, Tans SJ, Koenderink GH. 2022. Weak catch bonds make strong networks. Nature Materials. 21(9), 1019–1023. mla: Mulla, Yuval, et al. “Weak Catch Bonds Make Strong Networks.” Nature Materials, vol. 21, no. 9, Springer Nature, 2022, pp. 1019–23, doi:10.1038/s41563-022-01288-0. short: Y. Mulla, M. Avellaneda Sarrió, A. Roland, L. Baldauf, W. Jung, T. Kim, S.J. Tans, G.H. Koenderink, Nature Materials 21 (2022) 1019–1023. date_created: 2022-09-11T22:01:57Z date_published: 2022-09-01T00:00:00Z date_updated: 2023-08-03T14:08:47Z day: '01' department: - _id: MiSi doi: 10.1038/s41563-022-01288-0 external_id: isi: - '000844592000002' pmid: - '36008604' intvolume: ' 21' isi: 1 issue: '9' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1101/2020.07.27.219618 month: '09' oa: 1 oa_version: Preprint page: 1019-1023 pmid: 1 publication: Nature Materials publication_identifier: eissn: - 1476-4660 issn: - 1476-1122 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Weak catch bonds make strong networks type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 21 year: '2022' ... --- _id: '12119' abstract: - lang: eng text: Intravascular neutrophils and platelets collaborate in maintaining host integrity, but their interaction can also trigger thrombotic complications. We report here that cooperation between neutrophil and platelet lineages extends to the earliest stages of platelet formation by megakaryocytes in the bone marrow. Using intravital microscopy, we show that neutrophils “plucked” intravascular megakaryocyte extensions, termed proplatelets, to control platelet production. Following CXCR4-CXCL12-dependent migration towards perisinusoidal megakaryocytes, plucking neutrophils actively pulled on proplatelets and triggered myosin light chain and extracellular-signal-regulated kinase activation through reactive oxygen species. By these mechanisms, neutrophils accelerate proplatelet growth and facilitate continuous release of platelets in steady state. Following myocardial infarction, plucking neutrophils drove excessive release of young, reticulated platelets and boosted the risk of recurrent ischemia. Ablation of neutrophil plucking normalized thrombopoiesis and reduced recurrent thrombosis after myocardial infarction and thrombus burden in venous thrombosis. We establish neutrophil plucking as a target to reduce thromboischemic events. acknowledgement: "We thank Coung Kieu and Dominik van den Heuvel for excellent technical assistance. This work was supported by the German Research Foundation (PE2704/2-1, PE2704/3-1 to T.P., SFB 1123-project B06 to S.M., SFB1525 project A07 to D.S, TRR 332 project A7 to C.S., PO 2247/2-1 to A.P., SFB1116-project B11 to A.P. and B12 to M.K.), LMU Munich’s Institutional\r\nStrategy LMUexcellent within the framework of the German Excellence Initiative (No. 806 32 006 to T.P.), and by the German Centre for Cardiovascular Research (DZHK) to T.P. (Postdoc Start-up grant No. 100378833). This project has received funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program (grant agreement No. 833440 to S.M.). F.G. received funding from the European Union’s\r\nHorizon 2020 research and innovation program under the Marie Sk1odowska-Curie grant agreement no. 747687. A.H. was funded by RTI2018-095497-B-I00 from Ministerio de Ciencia e Innovacio´ n (MICINN), HR17_00527 from Fundacion La Caixa, and Transatlantic Network of Excellence (TNE-18CVD04) from the Leducq Foundation. The CNIC is supported by the MICINN and the Pro CNIC Foundation and is a Severo Ochoa Center of Excellence (CEX2020-001041-S). A.P. was supported by the Forschungskommission of the Medical Faculty of the Heinrich-Heine-Universität Düsseldorf (No. 18-2019 to A.P.). C.G. was supported by the Helmholtz Alliance ‘Aging and Metabolic Programming, AMPro,’ by the German Federal\r\nMinistry of Education and Research to the German Center for Diabetes Research (DZD), and by the Bavarian State Ministry of Health and Care through the research project DigiMed Bayern." article_processing_charge: No article_type: original author: - first_name: Tobias full_name: Petzold, Tobias last_name: Petzold - first_name: Zhe full_name: Zhang, Zhe last_name: Zhang - first_name: Iván full_name: Ballesteros, Iván last_name: Ballesteros - first_name: Inas full_name: Saleh, Inas last_name: Saleh - first_name: Amin full_name: Polzin, Amin last_name: Polzin - first_name: Manuela full_name: Thienel, Manuela last_name: Thienel - first_name: Lulu full_name: Liu, Lulu last_name: Liu - first_name: Qurrat full_name: Ul Ain, Qurrat last_name: Ul Ain - first_name: Vincent full_name: Ehreiser, Vincent last_name: Ehreiser - first_name: Christian full_name: Weber, Christian last_name: Weber - first_name: Badr full_name: Kilani, Badr last_name: Kilani - first_name: Pontus full_name: Mertsch, Pontus last_name: Mertsch - first_name: Jeremias full_name: Götschke, Jeremias last_name: Götschke - first_name: Sophie full_name: Cremer, Sophie last_name: Cremer - first_name: Wenwen full_name: Fu, Wenwen last_name: Fu - first_name: Michael full_name: Lorenz, Michael last_name: Lorenz - first_name: Hellen full_name: Ishikawa-Ankerhold, Hellen last_name: Ishikawa-Ankerhold - first_name: Elisabeth full_name: Raatz, Elisabeth last_name: Raatz - first_name: Shaza full_name: El-Nemr, Shaza last_name: El-Nemr - first_name: Agnes full_name: Görlach, Agnes last_name: Görlach - first_name: Esther full_name: Marhuenda, Esther last_name: Marhuenda - first_name: Konstantin full_name: Stark, Konstantin last_name: Stark - first_name: Joachim full_name: Pircher, Joachim last_name: Pircher - first_name: David full_name: Stegner, David last_name: Stegner - first_name: Christian full_name: Gieger, Christian last_name: Gieger - first_name: Marc full_name: Schmidt-Supprian, Marc last_name: Schmidt-Supprian - first_name: Florian R full_name: Gärtner, Florian R id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 - first_name: Isaac full_name: Almendros, Isaac last_name: Almendros - first_name: Malte full_name: Kelm, Malte last_name: Kelm - first_name: Christian full_name: Schulz, Christian last_name: Schulz - first_name: Andrés full_name: Hidalgo, Andrés last_name: Hidalgo - first_name: Steffen full_name: Massberg, Steffen last_name: Massberg citation: ama: Petzold T, Zhang Z, Ballesteros I, et al. Neutrophil “plucking” on megakaryocytes drives platelet production and boosts cardiovascular disease. Immunity. 2022;55(12):2285-2299.e7. doi:10.1016/j.immuni.2022.10.001 apa: Petzold, T., Zhang, Z., Ballesteros, I., Saleh, I., Polzin, A., Thienel, M., … Massberg, S. (2022). Neutrophil “plucking” on megakaryocytes drives platelet production and boosts cardiovascular disease. Immunity. Elsevier. https://doi.org/10.1016/j.immuni.2022.10.001 chicago: Petzold, Tobias, Zhe Zhang, Iván Ballesteros, Inas Saleh, Amin Polzin, Manuela Thienel, Lulu Liu, et al. “Neutrophil ‘Plucking’ on Megakaryocytes Drives Platelet Production and Boosts Cardiovascular Disease.” Immunity. Elsevier, 2022. https://doi.org/10.1016/j.immuni.2022.10.001. ieee: T. Petzold et al., “Neutrophil ‘plucking’ on megakaryocytes drives platelet production and boosts cardiovascular disease,” Immunity, vol. 55, no. 12. Elsevier, p. 2285–2299.e7, 2022. ista: Petzold T, Zhang Z, Ballesteros I, Saleh I, Polzin A, Thienel M, Liu L, Ul Ain Q, Ehreiser V, Weber C, Kilani B, Mertsch P, Götschke J, Cremer S, Fu W, Lorenz M, Ishikawa-Ankerhold H, Raatz E, El-Nemr S, Görlach A, Marhuenda E, Stark K, Pircher J, Stegner D, Gieger C, Schmidt-Supprian M, Gärtner FR, Almendros I, Kelm M, Schulz C, Hidalgo A, Massberg S. 2022. Neutrophil “plucking” on megakaryocytes drives platelet production and boosts cardiovascular disease. Immunity. 55(12), 2285–2299.e7. mla: Petzold, Tobias, et al. “Neutrophil ‘Plucking’ on Megakaryocytes Drives Platelet Production and Boosts Cardiovascular Disease.” Immunity, vol. 55, no. 12, Elsevier, 2022, p. 2285–2299.e7, doi:10.1016/j.immuni.2022.10.001. short: T. Petzold, Z. Zhang, I. Ballesteros, I. Saleh, A. Polzin, M. Thienel, L. Liu, Q. Ul Ain, V. Ehreiser, C. Weber, B. Kilani, P. Mertsch, J. Götschke, S. Cremer, W. Fu, M. Lorenz, H. Ishikawa-Ankerhold, E. Raatz, S. El-Nemr, A. Görlach, E. Marhuenda, K. Stark, J. Pircher, D. Stegner, C. Gieger, M. Schmidt-Supprian, F.R. Gärtner, I. Almendros, M. Kelm, C. Schulz, A. Hidalgo, S. Massberg, Immunity 55 (2022) 2285–2299.e7. date_created: 2023-01-12T11:56:54Z date_published: 2022-12-13T00:00:00Z date_updated: 2023-08-03T14:21:51Z day: '13' ddc: - '570' department: - _id: MiSi doi: 10.1016/j.immuni.2022.10.001 ec_funded: 1 external_id: isi: - '000922019600003' pmid: - '36272416' file: - access_level: open_access checksum: 073267a9c0ad9f85a650053bc7b23777 content_type: application/pdf creator: dernst date_created: 2023-01-23T10:18:48Z date_updated: 2023-01-23T10:18:48Z file_id: '12341' file_name: 2022_Immunity_Petzold.pdf file_size: 5299475 relation: main_file success: 1 file_date_updated: 2023-01-23T10:18:48Z has_accepted_license: '1' intvolume: ' 55' isi: 1 issue: '12' keyword: - Infectious Diseases - Immunology - Immunology and Allergy language: - iso: eng license: https://creativecommons.org/licenses/by-nc-nd/4.0/ month: '12' oa: 1 oa_version: Published Version page: 2285-2299.e7 pmid: 1 project: - _id: 260AA4E2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '747687' name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells publication: Immunity publication_identifier: issn: - 1074-7613 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Neutrophil “plucking” on megakaryocytes drives platelet production and boosts cardiovascular disease tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 55 year: '2022' ... --- _id: '12133' abstract: - lang: eng text: Social distancing is an effective way to prevent the spread of disease in societies, whereas infection elimination is a key element of organismal immunity. Here, we discuss how the study of social insects such as ants — which form a superorganism of unconditionally cooperative individuals and thus represent a level of organization that is intermediate between a classical society of individuals and an organism of cells — can help to determine common principles of disease defence across levels of organization. article_processing_charge: No article_type: letter_note author: - first_name: Sylvia full_name: Cremer, Sylvia id: 2F64EC8C-F248-11E8-B48F-1D18A9856A87 last_name: Cremer orcid: 0000-0002-2193-3868 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Cremer S, Sixt MK. Principles of disease defence in organisms, superorganisms and societies. Nature Reviews Immunology. 2022;22(12):713-714. doi:10.1038/s41577-022-00797-y apa: Cremer, S., & Sixt, M. K. (2022). Principles of disease defence in organisms, superorganisms and societies. Nature Reviews Immunology. Springer Nature. https://doi.org/10.1038/s41577-022-00797-y chicago: Cremer, Sylvia, and Michael K Sixt. “Principles of Disease Defence in Organisms, Superorganisms and Societies.” Nature Reviews Immunology. Springer Nature, 2022. https://doi.org/10.1038/s41577-022-00797-y. ieee: S. Cremer and M. K. Sixt, “Principles of disease defence in organisms, superorganisms and societies,” Nature Reviews Immunology, vol. 22, no. 12. Springer Nature, pp. 713–714, 2022. ista: Cremer S, Sixt MK. 2022. Principles of disease defence in organisms, superorganisms and societies. Nature Reviews Immunology. 22(12), 713–714. mla: Cremer, Sylvia, and Michael K. Sixt. “Principles of Disease Defence in Organisms, Superorganisms and Societies.” Nature Reviews Immunology, vol. 22, no. 12, Springer Nature, 2022, pp. 713–14, doi:10.1038/s41577-022-00797-y. short: S. Cremer, M.K. Sixt, Nature Reviews Immunology 22 (2022) 713–714. date_created: 2023-01-12T12:03:14Z date_published: 2022-12-01T00:00:00Z date_updated: 2023-08-04T08:53:32Z day: '01' department: - _id: SyCr - _id: MiSi doi: 10.1038/s41577-022-00797-y external_id: isi: - '000871836300001' pmid: - '36284178' intvolume: ' 22' isi: 1 issue: '12' keyword: - Energy Engineering and Power Technology - Fuel Technology language: - iso: eng month: '12' oa_version: None page: 713-714 pmid: 1 publication: Nature Reviews Immunology publication_identifier: eissn: - 1474-1741 issn: - 1474-1733 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Principles of disease defence in organisms, superorganisms and societies type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 22 year: '2022' ... --- _id: '12272' abstract: - lang: eng text: Reading, interpreting and crawling along gradients of chemotactic cues is one of the most complex questions in cell biology. In this issue, Georgantzoglou et al. (2022. J. Cell. Biol.https://doi.org/10.1083/jcb.202103207) use in vivo models to map the temporal sequence of how neutrophils respond to an acutely arising gradient of chemoattractant. article_number: e202206127 article_processing_charge: No article_type: original author: - first_name: Julian A full_name: Stopp, Julian A id: 489E3F00-F248-11E8-B48F-1D18A9856A87 last_name: Stopp - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Stopp JA, Sixt MK. Plan your trip before you leave: The neutrophils’ search-and-run journey. Journal of Cell Biology. 2022;221(8). doi:10.1083/jcb.202206127' apa: 'Stopp, J. A., & Sixt, M. K. (2022). Plan your trip before you leave: The neutrophils’ search-and-run journey. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.202206127' chicago: 'Stopp, Julian A, and Michael K Sixt. “Plan Your Trip before You Leave: The Neutrophils’ Search-and-Run Journey.” Journal of Cell Biology. Rockefeller University Press, 2022. https://doi.org/10.1083/jcb.202206127.' ieee: 'J. A. Stopp and M. K. Sixt, “Plan your trip before you leave: The neutrophils’ search-and-run journey,” Journal of Cell Biology, vol. 221, no. 8. Rockefeller University Press, 2022.' ista: 'Stopp JA, Sixt MK. 2022. Plan your trip before you leave: The neutrophils’ search-and-run journey. Journal of Cell Biology. 221(8), e202206127.' mla: 'Stopp, Julian A., and Michael K. Sixt. “Plan Your Trip before You Leave: The Neutrophils’ Search-and-Run Journey.” Journal of Cell Biology, vol. 221, no. 8, e202206127, Rockefeller University Press, 2022, doi:10.1083/jcb.202206127.' short: J.A. Stopp, M.K. Sixt, Journal of Cell Biology 221 (2022). date_created: 2023-01-16T10:01:08Z date_published: 2022-07-20T00:00:00Z date_updated: 2023-12-21T14:30:01Z day: '20' ddc: - '570' department: - _id: MiSi doi: 10.1083/jcb.202206127 external_id: isi: - '000874717200001' pmid: - '35856919' file: - access_level: open_access checksum: 6b1620743669679b48b9389bb40f5a11 content_type: application/pdf creator: dernst date_created: 2023-01-30T10:39:34Z date_updated: 2023-01-30T10:39:34Z file_id: '12451' file_name: 2022_JourCellBiology_Stopp.pdf file_size: 969969 relation: main_file success: 1 file_date_updated: 2023-01-30T10:39:34Z has_accepted_license: '1' intvolume: ' 221' isi: 1 issue: '8' keyword: - Cell Biology language: - iso: eng license: https://creativecommons.org/licenses/by-nc-sa/4.0/ month: '07' oa: 1 oa_version: Published Version pmid: 1 publication: Journal of Cell Biology publication_identifier: eissn: - 1540-8140 issn: - 0021-9525 publication_status: published publisher: Rockefeller University Press quality_controlled: '1' related_material: record: - id: '14697' relation: dissertation_contains status: public scopus_import: '1' status: public title: 'Plan your trip before you leave: The neutrophils’ search-and-run journey' tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 221 year: '2022' ... --- _id: '10703' abstract: - lang: eng text: 'When crawling through the body, leukocytes often traverse tissues that are densely packed with extracellular matrix and other cells, and this raises the question: How do leukocytes overcome compressive mechanical loads? Here, we show that the actin cortex of leukocytes is mechanoresponsive and that this responsiveness requires neither force sensing via the nucleus nor adhesive interactions with a substrate. Upon global compression of the cell body as well as local indentation of the plasma membrane, Wiskott-Aldrich syndrome protein (WASp) assembles into dot-like structures, providing activation platforms for Arp2/3 nucleated actin patches. These patches locally push against the external load, which can be obstructing collagen fibers or other cells, and thereby create space to facilitate forward locomotion. We show in vitro and in vivo that this WASp function is rate limiting for ameboid leukocyte migration in dense but not in loose environments and is required for trafficking through diverse tissues such as skin and lymph nodes.' acknowledged_ssus: - _id: LifeSc - _id: Bio - _id: EM-Fac acknowledgement: We thank N. Darwish-Miranda, F. Leite, F.P. Assen, and A. Eichner for advice and help with experiments. We thank J. Renkawitz, E. Kiermaier, A. Juanes Garcia, and M. Avellaneda for critical reading of the manuscript. We thank M. Driscoll for advice on fluorescent labeling of collagen gels. This research was supported by the Scientific Service Units (SSUs) of IST Austria through resources provided by Molecular Biology Services/Lab Support Facility (LSF)/Bioimaging Facility/Electron Microscopy Facility. This work was funded by grants from the European Research Council ( CoG 724373 ) and the Austrian Science Foundation (FWF) to M.S. F.G. received funding from the European Union’s Horizon 2020 research and innovation program under the Marie Skłodowska-Curie grant agreement no. 747687. article_processing_charge: No article_type: original author: - first_name: Florian full_name: Gaertner, Florian last_name: Gaertner - first_name: Patricia full_name: Reis-Rodrigues, Patricia last_name: Reis-Rodrigues - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Juan full_name: Aguilera, Juan last_name: Aguilera - first_name: Michael full_name: Riedl, Michael id: 3BE60946-F248-11E8-B48F-1D18A9856A87 last_name: Riedl orcid: 0000-0003-4844-6311 - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Saren full_name: Tasciyan, Saren id: 4323B49C-F248-11E8-B48F-1D18A9856A87 last_name: Tasciyan orcid: 0000-0003-1671-393X - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Vanessa full_name: Zheden, Vanessa id: 39C5A68A-F248-11E8-B48F-1D18A9856A87 last_name: Zheden orcid: 0000-0002-9438-4783 - first_name: Walter full_name: Kaufmann, Walter id: 3F99E422-F248-11E8-B48F-1D18A9856A87 last_name: Kaufmann orcid: 0000-0001-9735-5315 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Gaertner F, Reis-Rodrigues P, de Vries I, et al. WASp triggers mechanosensitive actin patches to facilitate immune cell migration in dense tissues. Developmental Cell. 2022;57(1):47-62.e9. doi:10.1016/j.devcel.2021.11.024 apa: Gaertner, F., Reis-Rodrigues, P., de Vries, I., Hons, M., Aguilera, J., Riedl, M., … Sixt, M. K. (2022). WASp triggers mechanosensitive actin patches to facilitate immune cell migration in dense tissues. Developmental Cell. Cell Press ; Elsevier. https://doi.org/10.1016/j.devcel.2021.11.024 chicago: Gaertner, Florian, Patricia Reis-Rodrigues, Ingrid de Vries, Miroslav Hons, Juan Aguilera, Michael Riedl, Alexander F Leithner, et al. “WASp Triggers Mechanosensitive Actin Patches to Facilitate Immune Cell Migration in Dense Tissues.” Developmental Cell. Cell Press ; Elsevier, 2022. https://doi.org/10.1016/j.devcel.2021.11.024. ieee: F. Gaertner et al., “WASp triggers mechanosensitive actin patches to facilitate immune cell migration in dense tissues,” Developmental Cell, vol. 57, no. 1. Cell Press ; Elsevier, p. 47–62.e9, 2022. ista: Gaertner F, Reis-Rodrigues P, de Vries I, Hons M, Aguilera J, Riedl M, Leithner AF, Tasciyan S, Kopf A, Merrin J, Zheden V, Kaufmann W, Hauschild R, Sixt MK. 2022. WASp triggers mechanosensitive actin patches to facilitate immune cell migration in dense tissues. Developmental Cell. 57(1), 47–62.e9. mla: Gaertner, Florian, et al. “WASp Triggers Mechanosensitive Actin Patches to Facilitate Immune Cell Migration in Dense Tissues.” Developmental Cell, vol. 57, no. 1, Cell Press ; Elsevier, 2022, p. 47–62.e9, doi:10.1016/j.devcel.2021.11.024. short: F. Gaertner, P. Reis-Rodrigues, I. de Vries, M. Hons, J. Aguilera, M. Riedl, A.F. Leithner, S. Tasciyan, A. Kopf, J. Merrin, V. Zheden, W. Kaufmann, R. Hauschild, M.K. Sixt, Developmental Cell 57 (2022) 47–62.e9. date_created: 2022-01-30T23:01:33Z date_published: 2022-01-10T00:00:00Z date_updated: 2024-03-27T23:30:23Z day: '10' ddc: - '570' department: - _id: MiSi - _id: EM-Fac - _id: NanoFab - _id: BjHo doi: 10.1016/j.devcel.2021.11.024 ec_funded: 1 external_id: isi: - '000768933800005' pmid: - '34919802' intvolume: ' 57' isi: 1 issue: '1' language: - iso: eng main_file_link: - open_access: '1' url: https://www.sciencedirect.com/science/article/pii/S1534580721009497 month: '01' oa: 1 oa_version: Published Version page: 47-62.e9 pmid: 1 project: - _id: 260AA4E2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '747687' name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: Developmental Cell publication_identifier: eissn: - 1878-1551 issn: - 1534-5807 publication_status: published publisher: Cell Press ; Elsevier quality_controlled: '1' related_material: record: - id: '12726' relation: dissertation_contains status: public - id: '14530' relation: dissertation_contains status: public - id: '12401' relation: dissertation_contains status: public scopus_import: '1' status: public title: WASp triggers mechanosensitive actin patches to facilitate immune cell migration in dense tissues tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 57 year: '2022' ... --- _id: '12401' abstract: - lang: eng text: "Detachment of the cancer cells from the bulk of the tumor is the first step of metastasis, which\r\nis the primary cause of cancer related deaths. It is unclear, which factors contribute to this step.\r\nRecent studies indicate a crucial role of the tumor microenvironment in malignant\r\ntransformation and metastasis. Studying cancer cell invasion and detachments quantitatively in\r\nthe context of its physiological microenvironment is technically challenging. Especially, precise\r\ncontrol of microenvironmental properties in vivo is currently not possible. Here, I studied the\r\nrole of microenvironment geometry in the invasion and detachment of cancer cells from the\r\nbulk with a simplistic and reductionist approach. In this approach, I engineered microfluidic\r\ndevices to mimic a pseudo 3D extracellular matrix environment, where I was able to\r\nquantitatively tune the geometrical configuration of the microenvironment and follow tumor\r\ncells with fluorescence live imaging. To aid quantitative analysis I developed a widely applicable\r\nsoftware application to automatically analyze and visualize particle tracking data.\r\nQuantitative analysis of tumor cell invasion in isotropic and anisotropic microenvironments\r\nshowed that heterogeneity in the microenvironment promotes faster invasion and more\r\nfrequent detachment of cells. These observations correlated with overall higher speed of cells at\r\nthe edge of the bulk of the cells. In heterogeneous microenvironments cells preferentially\r\npassed through larger pores, thus invading areas of least resistance and generating finger-like\r\ninvasive structures. The detachments occurred mostly at the tips of these structures.\r\nTo investigate the potential mechanism, we established a two dimensional model to simulate\r\nactive Brownian particles representing the cell nuclei dynamics. These simulations backed our in\r\nvitro observations without the need of precise fitting the simulation parameters. Our model\r\nsuggests the importance of the pore heterogeneity in the direction perpendicular to the\r\norientation of bias field (lateral heterogeneity), which causes the interface roughening." alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Saren full_name: Tasciyan, Saren id: 4323B49C-F248-11E8-B48F-1D18A9856A87 last_name: Tasciyan orcid: 0000-0003-1671-393X citation: ama: Tasciyan S. Role of microenvironment heterogeneity in cancer cell invasion. 2022. doi:10.15479/at:ista:12401 apa: Tasciyan, S. (2022). Role of microenvironment heterogeneity in cancer cell invasion. Institute of Science and Technology Austria. https://doi.org/10.15479/at:ista:12401 chicago: Tasciyan, Saren. “Role of Microenvironment Heterogeneity in Cancer Cell Invasion.” Institute of Science and Technology Austria, 2022. https://doi.org/10.15479/at:ista:12401. ieee: S. Tasciyan, “Role of microenvironment heterogeneity in cancer cell invasion,” Institute of Science and Technology Austria, 2022. ista: Tasciyan S. 2022. Role of microenvironment heterogeneity in cancer cell invasion. Institute of Science and Technology Austria. mla: Tasciyan, Saren. Role of Microenvironment Heterogeneity in Cancer Cell Invasion. Institute of Science and Technology Austria, 2022, doi:10.15479/at:ista:12401. short: S. Tasciyan, Role of Microenvironment Heterogeneity in Cancer Cell Invasion, Institute of Science and Technology Austria, 2022. date_created: 2023-01-26T11:55:16Z date_published: 2022-12-22T00:00:00Z date_updated: 2023-12-21T23:30:04Z day: '22' ddc: - '610' degree_awarded: PhD department: - _id: GradSch - _id: MiSi doi: 10.15479/at:ista:12401 file: - access_level: open_access checksum: cc4a2b4a7e3c4ee8ef7f2dbf909b12bd content_type: application/pdf creator: cchlebak date_created: 2023-01-26T11:58:14Z date_updated: 2023-12-21T23:30:03Z embargo: 2023-12-20 file_id: '12402' file_name: PhD-Thesis_Saren Tasciyan_formatted_aftercrash_fixed_600dpi_95pc_final_PDFA3b.pdf file_size: 42059787 relation: main_file - access_level: closed checksum: f1b4ca98b8ab0cb043b1830971e9bd9c content_type: application/x-zip-compressed creator: cchlebak date_created: 2023-01-26T12:00:10Z date_updated: 2023-12-21T23:30:03Z embargo_to: open_access file_id: '12403' file_name: Source Files - Saren Tasciyan - PhD Thesis.zip file_size: 261256696 relation: source_file file_date_updated: 2023-12-21T23:30:03Z has_accepted_license: '1' language: - iso: eng month: '12' oa: 1 oa_version: Published Version page: '105' publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria related_material: record: - id: '679' relation: part_of_dissertation status: public - id: '10703' relation: part_of_dissertation status: public - id: '9429' relation: part_of_dissertation status: public - id: '7885' relation: part_of_dissertation status: public status: public supervisor: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 title: Role of microenvironment heterogeneity in cancer cell invasion type: dissertation user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9 year: '2022' ... --- _id: '8988' abstract: - lang: eng text: The differentiation of cells depends on a precise control of their internal organization, which is the result of a complex dynamic interplay between the cytoskeleton, molecular motors, signaling molecules, and membranes. For example, in the developing neuron, the protein ADAP1 (ADP-ribosylation factor GTPase-activating protein [ArfGAP] with dual pleckstrin homology [PH] domains 1) has been suggested to control dendrite branching by regulating the small GTPase ARF6. Together with the motor protein KIF13B, ADAP1 is also thought to mediate delivery of the second messenger phosphatidylinositol (3,4,5)-trisphosphate (PIP3) to the axon tip, thus contributing to PIP3 polarity. However, what defines the function of ADAP1 and how its different roles are coordinated are still not clear. Here, we studied ADAP1’s functions using in vitro reconstitutions. We found that KIF13B transports ADAP1 along microtubules, but that PIP3 as well as PI(3,4)P2 act as stop signals for this transport instead of being transported. We also demonstrate that these phosphoinositides activate ADAP1’s enzymatic activity to catalyze GTP hydrolysis by ARF6. Together, our results support a model for the cellular function of ADAP1, where KIF13B transports ADAP1 until it encounters high PIP3/PI(3,4)P2 concentrations in the plasma membrane. Here, ADAP1 disassociates from the motor to inactivate ARF6, promoting dendrite branching. acknowledged_ssus: - _id: Bio - _id: LifeSc - _id: EM-Fac acknowledgement: "We thank Urban Bezeljak, Natalia Baranova, Mar Lopez-Pelegrin, Catarina Alcarva, and Victoria Faas for sharing reagents and helpful discussions. We thank Veronika Szentirmai for help with protein purifications. We thank Carrie Bernecky, Sascha Martens, and the M.L. lab for comments on the manuscript. We thank the bioimaging facility, the life science facility, and Armel Nicolas from the mass spec facility at the Institute of Science and Technology (IST) Austria for technical support. C.D. acknowledges funding from the IST fellowship program; this work was supported by Human Frontier Science Program Young Investigator Grant\r\nRGY0083/2016. " article_number: e2010054118 article_processing_charge: No article_type: original author: - first_name: Christian F full_name: Düllberg, Christian F id: 459064DC-F248-11E8-B48F-1D18A9856A87 last_name: Düllberg orcid: 0000-0001-6335-9748 - first_name: Albert full_name: Auer, Albert id: 3018E8C2-F248-11E8-B48F-1D18A9856A87 last_name: Auer orcid: 0000-0002-3580-2906 - first_name: Nikola full_name: Canigova, Nikola id: 3795523E-F248-11E8-B48F-1D18A9856A87 last_name: Canigova orcid: 0000-0002-8518-5926 - first_name: Katrin full_name: Loibl, Katrin id: 3760F32C-F248-11E8-B48F-1D18A9856A87 last_name: Loibl orcid: 0000-0002-2429-7668 - first_name: Martin full_name: Loose, Martin id: 462D4284-F248-11E8-B48F-1D18A9856A87 last_name: Loose orcid: 0000-0001-7309-9724 citation: ama: Düllberg CF, Auer A, Canigova N, Loibl K, Loose M. In vitro reconstitution reveals phosphoinositides as cargo-release factors and activators of the ARF6 GAP ADAP1. PNAS. 2021;118(1). doi:10.1073/pnas.2010054118 apa: Düllberg, C. F., Auer, A., Canigova, N., Loibl, K., & Loose, M. (2021). In vitro reconstitution reveals phosphoinositides as cargo-release factors and activators of the ARF6 GAP ADAP1. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.2010054118 chicago: Düllberg, Christian F, Albert Auer, Nikola Canigova, Katrin Loibl, and Martin Loose. “In Vitro Reconstitution Reveals Phosphoinositides as Cargo-Release Factors and Activators of the ARF6 GAP ADAP1.” PNAS. National Academy of Sciences, 2021. https://doi.org/10.1073/pnas.2010054118. ieee: C. F. Düllberg, A. Auer, N. Canigova, K. Loibl, and M. Loose, “In vitro reconstitution reveals phosphoinositides as cargo-release factors and activators of the ARF6 GAP ADAP1,” PNAS, vol. 118, no. 1. National Academy of Sciences, 2021. ista: Düllberg CF, Auer A, Canigova N, Loibl K, Loose M. 2021. In vitro reconstitution reveals phosphoinositides as cargo-release factors and activators of the ARF6 GAP ADAP1. PNAS. 118(1), e2010054118. mla: Düllberg, Christian F., et al. “In Vitro Reconstitution Reveals Phosphoinositides as Cargo-Release Factors and Activators of the ARF6 GAP ADAP1.” PNAS, vol. 118, no. 1, e2010054118, National Academy of Sciences, 2021, doi:10.1073/pnas.2010054118. short: C.F. Düllberg, A. Auer, N. Canigova, K. Loibl, M. Loose, PNAS 118 (2021). date_created: 2021-01-03T23:01:23Z date_published: 2021-01-05T00:00:00Z date_updated: 2023-08-04T11:20:46Z day: '05' department: - _id: MaLo - _id: MiSi doi: 10.1073/pnas.2010054118 external_id: isi: - '000607270100018' pmid: - '33443153' intvolume: ' 118' isi: 1 issue: '1' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1073/pnas.2010054118 month: '01' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 2599F062-B435-11E9-9278-68D0E5697425 grant_number: RGY0083/2016 name: Reconstitution of cell polarity and axis determination in a cell-free system publication: PNAS publication_identifier: eissn: - '10916490' issn: - '00278424' publication_status: published publisher: National Academy of Sciences quality_controlled: '1' scopus_import: '1' status: public title: In vitro reconstitution reveals phosphoinositides as cargo-release factors and activators of the ARF6 GAP ADAP1 type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 118 year: '2021' ... --- _id: '9259' abstract: - lang: eng text: Gradients of chemokines and growth factors guide migrating cells and morphogenetic processes. Migration of antigen-presenting dendritic cells from the interstitium into the lymphatic system is dependent on chemokine CCL21, which is secreted by endothelial cells of the lymphatic capillary, binds heparan sulfates and forms gradients decaying into the interstitium. Despite the importance of CCL21 gradients, and chemokine gradients in general, the mechanisms of gradient formation are unclear. Studies on fibroblast growth factors have shown that limited diffusion is crucial for gradient formation. Here, we used the mouse dermis as a model tissue to address the necessity of CCL21 anchoring to lymphatic capillary heparan sulfates in the formation of interstitial CCL21 gradients. Surprisingly, the absence of lymphatic endothelial heparan sulfates resulted only in a modest decrease of CCL21 levels at the lymphatic capillaries and did neither affect interstitial CCL21 gradient shape nor dendritic cell migration toward lymphatic capillaries. Thus, heparan sulfates at the level of the lymphatic endothelium are dispensable for the formation of a functional CCL21 gradient. acknowledgement: "This work was supported by Sigrid Juselius fellowship (KV), University of Helsinki 3-year research grant (KV), Academy of Finland Research fellow funding (315710, to KV), the European Research Council (ERC CoG 724373 to MS), and by the Austrian Science foundation (FWF) (Y564-B12 START award to MS).\r\nTaija Mäkinen is acknowledged for providing Prox1CreERT2 transgenic mice and Yu Yamaguchi for providing the conditional Ext1 mouse strain." article_number: '630002' article_processing_charge: No article_type: original author: - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Christine full_name: Moussion, Christine id: 3356F664-F248-11E8-B48F-1D18A9856A87 last_name: Moussion - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Vaahtomeri K, Moussion C, Hauschild R, Sixt MK. Shape and function of interstitial chemokine CCL21 gradients are independent of heparan sulfates produced by lymphatic endothelium. Frontiers in Immunology. 2021;12. doi:10.3389/fimmu.2021.630002 apa: Vaahtomeri, K., Moussion, C., Hauschild, R., & Sixt, M. K. (2021). Shape and function of interstitial chemokine CCL21 gradients are independent of heparan sulfates produced by lymphatic endothelium. Frontiers in Immunology. Frontiers. https://doi.org/10.3389/fimmu.2021.630002 chicago: Vaahtomeri, Kari, Christine Moussion, Robert Hauschild, and Michael K Sixt. “Shape and Function of Interstitial Chemokine CCL21 Gradients Are Independent of Heparan Sulfates Produced by Lymphatic Endothelium.” Frontiers in Immunology. Frontiers, 2021. https://doi.org/10.3389/fimmu.2021.630002. ieee: K. Vaahtomeri, C. Moussion, R. Hauschild, and M. K. Sixt, “Shape and function of interstitial chemokine CCL21 gradients are independent of heparan sulfates produced by lymphatic endothelium,” Frontiers in Immunology, vol. 12. Frontiers, 2021. ista: Vaahtomeri K, Moussion C, Hauschild R, Sixt MK. 2021. Shape and function of interstitial chemokine CCL21 gradients are independent of heparan sulfates produced by lymphatic endothelium. Frontiers in Immunology. 12, 630002. mla: Vaahtomeri, Kari, et al. “Shape and Function of Interstitial Chemokine CCL21 Gradients Are Independent of Heparan Sulfates Produced by Lymphatic Endothelium.” Frontiers in Immunology, vol. 12, 630002, Frontiers, 2021, doi:10.3389/fimmu.2021.630002. short: K. Vaahtomeri, C. Moussion, R. Hauschild, M.K. Sixt, Frontiers in Immunology 12 (2021). date_created: 2021-03-21T23:01:20Z date_published: 2021-02-25T00:00:00Z date_updated: 2023-08-07T14:18:26Z day: '25' ddc: - '570' department: - _id: MiSi - _id: Bio doi: 10.3389/fimmu.2021.630002 ec_funded: 1 external_id: isi: - '000627134400001' pmid: - '33717158' file: - access_level: open_access checksum: 663f5a48375e42afa4bfef58d42ec186 content_type: application/pdf creator: dernst date_created: 2021-03-22T12:08:26Z date_updated: 2021-03-22T12:08:26Z file_id: '9277' file_name: 2021_FrontiersImmumo_Vaahtomeri.pdf file_size: 3740146 relation: main_file success: 1 file_date_updated: 2021-03-22T12:08:26Z has_accepted_license: '1' intvolume: ' 12' isi: 1 language: - iso: eng month: '02' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and force transduction of migrating leukocytes publication: Frontiers in Immunology publication_identifier: eissn: - 1664-3224 publication_status: published publisher: Frontiers quality_controlled: '1' scopus_import: '1' status: public title: Shape and function of interstitial chemokine CCL21 gradients are independent of heparan sulfates produced by lymphatic endothelium tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 12 year: '2021' ... --- _id: '9294' abstract: - lang: eng text: In this issue of Developmental Cell, Doyle and colleagues identify periodic anterior contraction as a characteristic feature of fibroblasts and mesenchymal cancer cells embedded in 3D collagen gels. This contractile mechanism generates a matrix prestrain required for crawling in fibrous 3D environments. article_processing_charge: No article_type: original author: - first_name: Florian R full_name: Gärtner, Florian R id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Gärtner FR, Sixt MK. Engaging the front wheels to drive through fibrous terrain. Developmental Cell. 2021;56(6):723-725. doi:10.1016/j.devcel.2021.03.002 apa: Gärtner, F. R., & Sixt, M. K. (2021). Engaging the front wheels to drive through fibrous terrain. Developmental Cell. Elsevier. https://doi.org/10.1016/j.devcel.2021.03.002 chicago: Gärtner, Florian R, and Michael K Sixt. “Engaging the Front Wheels to Drive through Fibrous Terrain.” Developmental Cell. Elsevier, 2021. https://doi.org/10.1016/j.devcel.2021.03.002. ieee: F. R. Gärtner and M. K. Sixt, “Engaging the front wheels to drive through fibrous terrain,” Developmental Cell, vol. 56, no. 6. Elsevier, pp. 723–725, 2021. ista: Gärtner FR, Sixt MK. 2021. Engaging the front wheels to drive through fibrous terrain. Developmental Cell. 56(6), 723–725. mla: Gärtner, Florian R., and Michael K. Sixt. “Engaging the Front Wheels to Drive through Fibrous Terrain.” Developmental Cell, vol. 56, no. 6, Elsevier, 2021, pp. 723–25, doi:10.1016/j.devcel.2021.03.002. short: F.R. Gärtner, M.K. Sixt, Developmental Cell 56 (2021) 723–725. date_created: 2021-03-28T22:01:41Z date_published: 2021-03-22T00:00:00Z date_updated: 2023-08-07T14:26:47Z day: '22' department: - _id: MiSi doi: 10.1016/j.devcel.2021.03.002 external_id: isi: - '000631681200004' pmid: - '33756118' intvolume: ' 56' isi: 1 issue: '6' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.devcel.2021.03.002 month: '03' oa: 1 oa_version: Published Version page: 723-725 pmid: 1 publication: Developmental Cell publication_identifier: eissn: - '18781551' issn: - '15345807' publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Engaging the front wheels to drive through fibrous terrain type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 56 year: '2021' ... --- _id: '9822' abstract: - lang: eng text: Attachment of adhesive molecules on cell culture surfaces to restrict cell adhesion to defined areas and shapes has been vital for the progress of in vitro research. In currently existing patterning methods, a combination of pattern properties such as stability, precision, specificity, high-throughput outcome, and spatiotemporal control is highly desirable but challenging to achieve. Here, we introduce a versatile and high-throughput covalent photoimmobilization technique, comprising a light-dose-dependent patterning step and a subsequent functionalization of the pattern via click chemistry. This two-step process is feasible on arbitrary surfaces and allows for generation of sustainable patterns and gradients. The method is validated in different biological systems by patterning adhesive ligands on cell-repellent surfaces, thereby constraining the growth and migration of cells to the designated areas. We then implement a sequential photopatterning approach by adding a second switchable patterning step, allowing for spatiotemporal control over two distinct surface patterns. As a proof of concept, we reconstruct the dynamics of the tip/stalk cell switch during angiogenesis. Our results show that the spatiotemporal control provided by our “sequential photopatterning” system is essential for mimicking dynamic biological processes and that our innovative approach has great potential for further applications in cell science. acknowledgement: We would like to thank Charlott Leu for the production of our chromium wafers, Louise Ritter for her contribution of the IF stainings in Figure 4, Shokoufeh Teymouri for her help with the Bioinert coated slides, and finally Prof. Dr. Joachim Rädler for his valuable scientific guidance. article_processing_charge: Yes (in subscription journal) article_type: original author: - first_name: Themistoklis full_name: Zisis, Themistoklis last_name: Zisis - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Miriam full_name: Balles, Miriam last_name: Balles - first_name: Maibritt full_name: Kretschmer, Maibritt last_name: Kretschmer - first_name: Maria full_name: Nemethova, Maria id: 34E27F1C-F248-11E8-B48F-1D18A9856A87 last_name: Nemethova - first_name: Remy P full_name: Chait, Remy P id: 3464AE84-F248-11E8-B48F-1D18A9856A87 last_name: Chait orcid: 0000-0003-0876-3187 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Janina full_name: Lange, Janina last_name: Lange - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-4561-241X - first_name: Stefan full_name: Zahler, Stefan last_name: Zahler citation: ama: Zisis T, Schwarz J, Balles M, et al. Sequential and switchable patterning for studying cellular processes under spatiotemporal control. ACS Applied Materials and Interfaces. 2021;13(30):35545–35560. doi:10.1021/acsami.1c09850 apa: Zisis, T., Schwarz, J., Balles, M., Kretschmer, M., Nemethova, M., Chait, R. P., … Zahler, S. (2021). Sequential and switchable patterning for studying cellular processes under spatiotemporal control. ACS Applied Materials and Interfaces. American Chemical Society. https://doi.org/10.1021/acsami.1c09850 chicago: Zisis, Themistoklis, Jan Schwarz, Miriam Balles, Maibritt Kretschmer, Maria Nemethova, Remy P Chait, Robert Hauschild, et al. “Sequential and Switchable Patterning for Studying Cellular Processes under Spatiotemporal Control.” ACS Applied Materials and Interfaces. American Chemical Society, 2021. https://doi.org/10.1021/acsami.1c09850. ieee: T. Zisis et al., “Sequential and switchable patterning for studying cellular processes under spatiotemporal control,” ACS Applied Materials and Interfaces, vol. 13, no. 30. American Chemical Society, pp. 35545–35560, 2021. ista: Zisis T, Schwarz J, Balles M, Kretschmer M, Nemethova M, Chait RP, Hauschild R, Lange J, Guet CC, Sixt MK, Zahler S. 2021. Sequential and switchable patterning for studying cellular processes under spatiotemporal control. ACS Applied Materials and Interfaces. 13(30), 35545–35560. mla: Zisis, Themistoklis, et al. “Sequential and Switchable Patterning for Studying Cellular Processes under Spatiotemporal Control.” ACS Applied Materials and Interfaces, vol. 13, no. 30, American Chemical Society, 2021, pp. 35545–35560, doi:10.1021/acsami.1c09850. short: T. Zisis, J. Schwarz, M. Balles, M. Kretschmer, M. Nemethova, R.P. Chait, R. Hauschild, J. Lange, C.C. Guet, M.K. Sixt, S. Zahler, ACS Applied Materials and Interfaces 13 (2021) 35545–35560. date_created: 2021-08-08T22:01:28Z date_published: 2021-08-04T00:00:00Z date_updated: 2023-08-10T14:22:48Z day: '04' ddc: - '620' - '570' department: - _id: MiSi - _id: GaTk - _id: Bio - _id: CaGu doi: 10.1021/acsami.1c09850 ec_funded: 1 external_id: isi: - '000683741400026' pmid: - '34283577' file: - access_level: open_access checksum: b043a91d9f9200e467b970b692687ed3 content_type: application/pdf creator: asandaue date_created: 2021-08-09T09:44:03Z date_updated: 2021-08-09T09:44:03Z file_id: '9833' file_name: 2021_ACSAppliedMaterialsAndInterfaces_Zisis.pdf file_size: 7123293 relation: main_file success: 1 file_date_updated: 2021-08-09T09:44:03Z has_accepted_license: '1' intvolume: ' 13' isi: 1 issue: '30' language: - iso: eng month: '08' oa: 1 oa_version: Published Version page: 35545–35560 pmid: 1 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: ACS Applied Materials and Interfaces publication_identifier: eissn: - '19448252' issn: - '19448244' publication_status: published publisher: American Chemical Society quality_controlled: '1' scopus_import: '1' status: public title: Sequential and switchable patterning for studying cellular processes under spatiotemporal control tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 13 year: '2021' ... --- _id: '10834' abstract: - lang: eng text: Hematopoietic-specific protein 1 (Hem1) is an essential subunit of the WAVE regulatory complex (WRC) in immune cells. WRC is crucial for Arp2/3 complex activation and the protrusion of branched actin filament networks. Moreover, Hem1 loss of function in immune cells causes autoimmune diseases in humans. Here, we show that genetic removal of Hem1 in macrophages diminishes frequency and efficacy of phagocytosis as well as phagocytic cup formation in addition to defects in lamellipodial protrusion and migration. Moreover, Hem1-null macrophages displayed strong defects in cell adhesion despite unaltered podosome formation and concomitant extracellular matrix degradation. Specifically, dynamics of both adhesion and de-adhesion as well as concomitant phosphorylation of paxillin and focal adhesion kinase (FAK) were significantly compromised. Accordingly, disruption of WRC function in non-hematopoietic cells coincided with both defects in adhesion turnover and altered FAK and paxillin phosphorylation. Consistently, platelets exhibited reduced adhesion and diminished integrin αIIbβ3 activation upon WRC removal. Interestingly, adhesion phenotypes, but not lamellipodia formation, were partially rescued by small molecule activation of FAK. A full rescue of the phenotype, including lamellipodia formation, required not only the presence of WRCs but also their binding to and activation by Rac. Collectively, our results uncover that WRC impacts on integrin-dependent processes in a FAK-dependent manner, controlling formation and dismantling of adhesions, relevant for properly grabbing onto extracellular surfaces and particles during cell edge expansion, like in migration or phagocytosis. acknowledgement: We are grateful to Silvia Prettin, Ina Schleicher, and Petra Hagendorff for expert technical assistance; David Dettbarn for animal keeping and breeding; and Lothar Gröbe and Maria Höxter for cell sorting. We also thank Werner Tegge for peptides and Giorgio Scita for antibodies. This work was supported, in part, by the Deutsche Forschungsgemeinschaft (DFG), Priority Programm SPP1150 (to T.E.B.S., K.R., and M. Sixt), and by DFG grant GRK2223/1 (to K.R.). T.E.B.S. acknowledges support by the Helmholtz Society through HGF impulse fund W2/W3-066 and M. Schnoor by the Mexican Council for Science and Technology (CONACyT, 284292 ), Fund SEP-Cinvestav ( 108 ), and the Royal Society, UK (Newton Advanced Fellowship, NAF/R1/180017 ). article_processing_charge: No article_type: original author: - first_name: Stephanie full_name: Stahnke, Stephanie last_name: Stahnke - first_name: Hermann full_name: Döring, Hermann last_name: Döring - first_name: Charly full_name: Kusch, Charly last_name: Kusch - first_name: David J.J. full_name: de Gorter, David J.J. last_name: de Gorter - first_name: Sebastian full_name: Dütting, Sebastian last_name: Dütting - first_name: Aleks full_name: Guledani, Aleks last_name: Guledani - first_name: Irina full_name: Pleines, Irina last_name: Pleines - first_name: Michael full_name: Schnoor, Michael last_name: Schnoor - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Robert full_name: Geffers, Robert last_name: Geffers - first_name: Manfred full_name: Rohde, Manfred last_name: Rohde - first_name: Mathias full_name: Müsken, Mathias last_name: Müsken - first_name: Frieda full_name: Kage, Frieda last_name: Kage - first_name: Anika full_name: Steffen, Anika last_name: Steffen - first_name: Jan full_name: Faix, Jan last_name: Faix - first_name: Bernhard full_name: Nieswandt, Bernhard last_name: Nieswandt - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner - first_name: Theresia E.B. full_name: Stradal, Theresia E.B. last_name: Stradal citation: ama: Stahnke S, Döring H, Kusch C, et al. Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis, and integrin-mediated adhesion. Current Biology. 2021;31(10):2051-2064.e8. doi:10.1016/j.cub.2021.02.043 apa: Stahnke, S., Döring, H., Kusch, C., de Gorter, D. J. J., Dütting, S., Guledani, A., … Stradal, T. E. B. (2021). Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis, and integrin-mediated adhesion. Current Biology. Elsevier. https://doi.org/10.1016/j.cub.2021.02.043 chicago: Stahnke, Stephanie, Hermann Döring, Charly Kusch, David J.J. de Gorter, Sebastian Dütting, Aleks Guledani, Irina Pleines, et al. “Loss of Hem1 Disrupts Macrophage Function and Impacts Migration, Phagocytosis, and Integrin-Mediated Adhesion.” Current Biology. Elsevier, 2021. https://doi.org/10.1016/j.cub.2021.02.043. ieee: S. Stahnke et al., “Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis, and integrin-mediated adhesion,” Current Biology, vol. 31, no. 10. Elsevier, p. 2051–2064.e8, 2021. ista: Stahnke S, Döring H, Kusch C, de Gorter DJJ, Dütting S, Guledani A, Pleines I, Schnoor M, Sixt MK, Geffers R, Rohde M, Müsken M, Kage F, Steffen A, Faix J, Nieswandt B, Rottner K, Stradal TEB. 2021. Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis, and integrin-mediated adhesion. Current Biology. 31(10), 2051–2064.e8. mla: Stahnke, Stephanie, et al. “Loss of Hem1 Disrupts Macrophage Function and Impacts Migration, Phagocytosis, and Integrin-Mediated Adhesion.” Current Biology, vol. 31, no. 10, Elsevier, 2021, p. 2051–2064.e8, doi:10.1016/j.cub.2021.02.043. short: S. Stahnke, H. Döring, C. Kusch, D.J.J. de Gorter, S. Dütting, A. Guledani, I. Pleines, M. Schnoor, M.K. Sixt, R. Geffers, M. Rohde, M. Müsken, F. Kage, A. Steffen, J. Faix, B. Nieswandt, K. Rottner, T.E.B. Stradal, Current Biology 31 (2021) 2051–2064.e8. date_created: 2022-03-08T07:51:04Z date_published: 2021-05-24T00:00:00Z date_updated: 2023-08-17T07:01:14Z day: '24' department: - _id: MiSi doi: 10.1016/j.cub.2021.02.043 external_id: isi: - '000654652200002' pmid: - '33711252' intvolume: ' 31' isi: 1 issue: '10' keyword: - General Agricultural and Biological Sciences - General Biochemistry - Genetics and Molecular Biology language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1101/2020.03.24.005835 month: '05' oa: 1 oa_version: Preprint page: 2051-2064.e8 pmid: 1 publication: Current Biology publication_identifier: issn: - 0960-9822 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis, and integrin-mediated adhesion type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 31 year: '2021' ... --- _id: '9094' abstract: - lang: eng text: Dendritic cells (DCs) are crucial for the priming of naive T cells and the initiation of adaptive immunity. Priming is initiated at a heterologous cell–cell contact, the immunological synapse (IS). While it is established that F-actin dynamics regulates signaling at the T cell side of the contact, little is known about the cytoskeletal contribution on the DC side. Here, we show that the DC actin cytoskeleton is decisive for the formation of a multifocal synaptic structure, which correlates with T cell priming efficiency. DC actin at the IS appears in transient foci that are dynamized by the WAVE regulatory complex (WRC). The absence of the WRC in DCs leads to stabilized contacts with T cells, caused by an increase in ICAM1-integrin–mediated cell–cell adhesion. This results in lower numbers of activated and proliferating T cells, demonstrating an important role for DC actin in the regulation of immune synapse functionality. article_number: e202006081 article_processing_charge: No article_type: original author: - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: LM full_name: Altenburger, LM last_name: Altenburger - first_name: R full_name: Hauschild, R last_name: Hauschild - first_name: Frank P full_name: Assen, Frank P id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87 last_name: Assen orcid: 0000-0003-3470-6119 - first_name: K full_name: Rottner, K last_name: Rottner - first_name: Stradal full_name: TEB, Stradal last_name: TEB - first_name: A full_name: Diz-Muñoz, A last_name: Diz-Muñoz - first_name: JV full_name: Stein, JV last_name: Stein - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Leithner AF, Altenburger L, Hauschild R, et al. Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse. Journal of Cell Biology. 2021;220(4). doi:10.1083/jcb.202006081 apa: Leithner, A. F., Altenburger, L., Hauschild, R., Assen, F. P., Rottner, K., TEB, S., … Sixt, M. K. (2021). Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.202006081 chicago: Leithner, Alexander F, LM Altenburger, R Hauschild, Frank P Assen, K Rottner, Stradal TEB, A Diz-Muñoz, JV Stein, and Michael K Sixt. “Dendritic Cell Actin Dynamics Control Contact Duration and Priming Efficiency at the Immunological Synapse.” Journal of Cell Biology. Rockefeller University Press, 2021. https://doi.org/10.1083/jcb.202006081. ieee: A. F. Leithner et al., “Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse,” Journal of Cell Biology, vol. 220, no. 4. Rockefeller University Press, 2021. ista: Leithner AF, Altenburger L, Hauschild R, Assen FP, Rottner K, TEB S, Diz-Muñoz A, Stein J, Sixt MK. 2021. Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse. Journal of Cell Biology. 220(4), e202006081. mla: Leithner, Alexander F., et al. “Dendritic Cell Actin Dynamics Control Contact Duration and Priming Efficiency at the Immunological Synapse.” Journal of Cell Biology, vol. 220, no. 4, e202006081, Rockefeller University Press, 2021, doi:10.1083/jcb.202006081. short: A.F. Leithner, L. Altenburger, R. Hauschild, F.P. Assen, K. Rottner, S. TEB, A. Diz-Muñoz, J. Stein, M.K. Sixt, Journal of Cell Biology 220 (2021). date_created: 2021-02-05T10:08:04Z date_published: 2021-04-05T00:00:00Z date_updated: 2023-09-05T13:57:53Z day: '05' ddc: - '570' department: - _id: MiSi doi: 10.1083/jcb.202006081 external_id: isi: - '000626365700001' pmid: - '33533935' file: - access_level: open_access checksum: 843ebc153847c8626e13c9c5ce71d533 content_type: application/pdf creator: dernst date_created: 2022-05-12T14:16:21Z date_updated: 2022-05-12T14:16:21Z file_id: '11367' file_name: 2021_JournCellBiology_Leithner.pdf file_size: 5102328 relation: main_file success: 1 file_date_updated: 2022-05-12T14:16:21Z has_accepted_license: '1' intvolume: ' 220' isi: 1 issue: '4' language: - iso: eng month: '04' oa: 1 oa_version: Published Version pmid: 1 publication: Journal of Cell Biology publication_identifier: eissn: - 1540-8140 issn: - 0021-9525 publication_status: published publisher: Rockefeller University Press quality_controlled: '1' scopus_import: '1' status: public title: Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 220 year: '2021' ... --- _id: '9429' abstract: - lang: eng text: De novo loss of function mutations in the ubiquitin ligase-encoding gene Cullin3 lead to autism spectrum disorder (ASD). In mouse, constitutive haploinsufficiency leads to motor coordination deficits as well as ASD-relevant social and cognitive impairments. However, induction of Cul3 haploinsufficiency later in life does not lead to ASD-relevant behaviors, pointing to an important role of Cul3 during a critical developmental window. Here we show that Cul3 is essential to regulate neuronal migration and, therefore, constitutive Cul3 heterozygous mutant mice display cortical lamination abnormalities. At the molecular level, we found that Cul3 controls neuronal migration by tightly regulating the amount of Plastin3 (Pls3), a previously unrecognized player of neural migration. Furthermore, we found that Pls3 cell-autonomously regulates cell migration by regulating actin cytoskeleton organization, and its levels are inversely proportional to neural migration speed. Finally, we provide evidence that cellular phenotypes associated with autism-linked gene haploinsufficiency can be rescued by transcriptional activation of the intact allele in vitro, offering a proof of concept for a potential therapeutic approach for ASDs. acknowledged_ssus: - _id: PreCl acknowledgement: We thank A. Coll Manzano, F. Freeman, M. Ladron de Guevara, and A. Ç. Yahya for technical assistance, S. Deixler, A. Lepold, and A. Schlerka for the management of our animal colony, as well as M. Schunn and the Preclinical Facility team for technical assistance. We thank K. Heesom and her team at the University of Bristol Proteomics Facility for the proteomics sample preparation, data generation, and analysis support. We thank Y. B. Simon for kindly providing the plasmid for lentiviral labeling. Further, we thank M. Sixt for his advice regarding cell migration and the fruitful discussions. This work was supported by the ISTPlus postdoctoral fellowship (Grant Agreement No. 754411) to B.B., by the European Union’s Horizon 2020 research and innovation program (ERC) grant 715508 (REVERSEAUTISM), and by the Austrian Science Fund (FWF) to G.N. (DK W1232-B24 and SFB F7807-B) and to J.G.D (I3600-B27). article_number: '3058' article_processing_charge: No article_type: original author: - first_name: Jasmin full_name: Morandell, Jasmin id: 4739D480-F248-11E8-B48F-1D18A9856A87 last_name: Morandell - first_name: Lena A full_name: Schwarz, Lena A id: 29A8453C-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Bernadette full_name: Basilico, Bernadette id: 36035796-5ACA-11E9-A75E-7AF2E5697425 last_name: Basilico orcid: 0000-0003-1843-3173 - first_name: Saren full_name: Tasciyan, Saren id: 4323B49C-F248-11E8-B48F-1D18A9856A87 last_name: Tasciyan orcid: 0000-0003-1671-393X - first_name: Georgi A full_name: Dimchev, Georgi A id: 38C393BE-F248-11E8-B48F-1D18A9856A87 last_name: Dimchev orcid: 0000-0001-8370-6161 - first_name: Armel full_name: Nicolas, Armel id: 2A103192-F248-11E8-B48F-1D18A9856A87 last_name: Nicolas - first_name: Christoph M full_name: Sommer, Christoph M id: 4DF26D8C-F248-11E8-B48F-1D18A9856A87 last_name: Sommer orcid: 0000-0003-1216-9105 - first_name: Caroline full_name: Kreuzinger, Caroline id: 382077BA-F248-11E8-B48F-1D18A9856A87 last_name: Kreuzinger - first_name: Christoph full_name: Dotter, Christoph id: 4C66542E-F248-11E8-B48F-1D18A9856A87 last_name: Dotter orcid: 0000-0002-9033-9096 - first_name: Lisa full_name: Knaus, Lisa id: 3B2ABCF4-F248-11E8-B48F-1D18A9856A87 last_name: Knaus - first_name: Zoe full_name: Dobler, Zoe id: D23090A2-9057-11EA-883A-A8396FC7A38F last_name: Dobler - first_name: Emanuele full_name: Cacci, Emanuele last_name: Cacci - first_name: Florian KM full_name: Schur, Florian KM id: 48AD8942-F248-11E8-B48F-1D18A9856A87 last_name: Schur orcid: 0000-0003-4790-8078 - first_name: Johann G full_name: Danzl, Johann G id: 42EFD3B6-F248-11E8-B48F-1D18A9856A87 last_name: Danzl orcid: 0000-0001-8559-3973 - first_name: Gaia full_name: Novarino, Gaia id: 3E57A680-F248-11E8-B48F-1D18A9856A87 last_name: Novarino orcid: 0000-0002-7673-7178 citation: ama: Morandell J, Schwarz LA, Basilico B, et al. Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development. Nature Communications. 2021;12(1). doi:10.1038/s41467-021-23123-x apa: Morandell, J., Schwarz, L. A., Basilico, B., Tasciyan, S., Dimchev, G. A., Nicolas, A., … Novarino, G. (2021). Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-021-23123-x chicago: Morandell, Jasmin, Lena A Schwarz, Bernadette Basilico, Saren Tasciyan, Georgi A Dimchev, Armel Nicolas, Christoph M Sommer, et al. “Cul3 Regulates Cytoskeleton Protein Homeostasis and Cell Migration during a Critical Window of Brain Development.” Nature Communications. Springer Nature, 2021. https://doi.org/10.1038/s41467-021-23123-x. ieee: J. Morandell et al., “Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development,” Nature Communications, vol. 12, no. 1. Springer Nature, 2021. ista: Morandell J, Schwarz LA, Basilico B, Tasciyan S, Dimchev GA, Nicolas A, Sommer CM, Kreuzinger C, Dotter C, Knaus L, Dobler Z, Cacci E, Schur FK, Danzl JG, Novarino G. 2021. Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development. Nature Communications. 12(1), 3058. mla: Morandell, Jasmin, et al. “Cul3 Regulates Cytoskeleton Protein Homeostasis and Cell Migration during a Critical Window of Brain Development.” Nature Communications, vol. 12, no. 1, 3058, Springer Nature, 2021, doi:10.1038/s41467-021-23123-x. short: J. Morandell, L.A. Schwarz, B. Basilico, S. Tasciyan, G.A. Dimchev, A. Nicolas, C.M. Sommer, C. Kreuzinger, C. Dotter, L. Knaus, Z. Dobler, E. Cacci, F.K. Schur, J.G. Danzl, G. Novarino, Nature Communications 12 (2021). date_created: 2021-05-28T11:49:46Z date_published: 2021-05-24T00:00:00Z date_updated: 2024-03-27T23:30:23Z day: '24' ddc: - '572' department: - _id: GaNo - _id: JoDa - _id: FlSc - _id: MiSi - _id: LifeSc - _id: Bio doi: 10.1038/s41467-021-23123-x ec_funded: 1 external_id: isi: - '000658769900010' file: - access_level: open_access checksum: 337e0f7959c35ec959984cacdcb472ba content_type: application/pdf creator: kschuh date_created: 2021-05-28T12:39:43Z date_updated: 2021-05-28T12:39:43Z file_id: '9430' file_name: 2021_NatureCommunications_Morandell.pdf file_size: 9358599 relation: main_file success: 1 file_date_updated: 2021-05-28T12:39:43Z has_accepted_license: '1' intvolume: ' 12' isi: 1 issue: '1' keyword: - General Biochemistry - Genetics and Molecular Biology language: - iso: eng month: '05' oa: 1 oa_version: Published Version project: - _id: 260C2330-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '754411' name: ISTplus - Postdoctoral Fellowships - _id: 25444568-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '715508' name: Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo and in vitro Models - _id: 2548AE96-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: W1232-B24 name: Molecular Drug Targets - _id: 05A0D778-7A3F-11EA-A408-12923DDC885E grant_number: F07807 name: Neural stem cells in autism and epilepsy - _id: 265CB4D0-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: I03600 name: Optical control of synaptic function via adhesion molecules publication: Nature Communications publication_identifier: eissn: - 2041-1723 publication_status: published publisher: Springer Nature quality_controlled: '1' related_material: link: - relation: press_release url: https://ist.ac.at/en/news/defective-gene-slows-down-brain-cells/ record: - id: '7800' relation: earlier_version status: public - id: '12401' relation: dissertation_contains status: public status: public title: Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 12 year: '2021' ... --- _id: '10307' abstract: - lang: eng text: Bacteria-host interactions represent a continuous trade-off between benefit and risk. Thus, the host immune response is faced with a non-trivial problem – accommodate beneficial commensals and remove harmful pathogens. This is especially difficult as molecular patterns, such as lipopolysaccharide or specific surface organelles such as pili, are conserved in both, commensal and pathogenic bacteria. Type 1 pili, tightly regulated by phase variation, are considered an important virulence factor of pathogenic bacteria as they facilitate invasion into host cells. While invasion represents a de facto passive mechanism for pathogens to escape the host immune response, we demonstrate a fundamental role of type 1 pili as active modulators of the innate and adaptive immune response. acknowledged_ssus: - _id: LifeSc - _id: Bio - _id: PreCl - _id: EM-Fac alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Kathrin full_name: Tomasek, Kathrin id: 3AEC8556-F248-11E8-B48F-1D18A9856A87 last_name: Tomasek orcid: 0000-0003-3768-877X citation: ama: Tomasek K. Pathogenic Escherichia coli hijack the host immune response. 2021. doi:10.15479/at:ista:10307 apa: Tomasek, K. (2021). Pathogenic Escherichia coli hijack the host immune response. Institute of Science and Technology Austria. https://doi.org/10.15479/at:ista:10307 chicago: Tomasek, Kathrin. “Pathogenic Escherichia Coli Hijack the Host Immune Response.” Institute of Science and Technology Austria, 2021. https://doi.org/10.15479/at:ista:10307. ieee: K. Tomasek, “Pathogenic Escherichia coli hijack the host immune response,” Institute of Science and Technology Austria, 2021. ista: Tomasek K. 2021. Pathogenic Escherichia coli hijack the host immune response. Institute of Science and Technology Austria. mla: Tomasek, Kathrin. Pathogenic Escherichia Coli Hijack the Host Immune Response. Institute of Science and Technology Austria, 2021, doi:10.15479/at:ista:10307. short: K. Tomasek, Pathogenic Escherichia Coli Hijack the Host Immune Response, Institute of Science and Technology Austria, 2021. date_created: 2021-11-18T15:05:06Z date_published: 2021-11-18T00:00:00Z date_updated: 2023-09-07T13:34:38Z day: '18' ddc: - '570' degree_awarded: PhD department: - _id: MiSi - _id: CaGu - _id: GradSch doi: 10.15479/at:ista:10307 file: - access_level: open_access checksum: b39c9e0ef18d0484d537a67551effd02 content_type: application/pdf creator: ktomasek date_created: 2021-11-18T15:07:31Z date_updated: 2022-12-20T23:30:05Z embargo: 2022-11-18 file_id: '10308' file_name: ThesisTomasekKathrin.pdf file_size: 13266088 relation: main_file - access_level: closed checksum: c0c440ee9e5ef1102a518a4f9f023e7c content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document creator: ktomasek date_created: 2021-11-18T15:07:46Z date_updated: 2022-12-20T23:30:05Z embargo_to: open_access file_id: '10309' file_name: ThesisTomasekKathrin.docx file_size: 7539509 relation: source_file file_date_updated: 2022-12-20T23:30:05Z has_accepted_license: '1' language: - iso: eng month: '11' oa: 1 oa_version: Published Version page: '73' publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria related_material: record: - id: '10316' relation: part_of_dissertation status: public status: public supervisor: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-4561-241X - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 title: Pathogenic Escherichia coli hijack the host immune response type: dissertation user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 year: '2021' ... --- _id: '10316' abstract: - lang: eng text: A key attribute of persistent or recurring bacterial infections is the ability of the pathogen to evade the host’s immune response. Many Enterobacteriaceae express type 1 pili, a pre-adapted virulence trait, to invade host epithelial cells and establish persistent infections. However, the molecular mechanisms and strategies by which bacteria actively circumvent the immune response of the host remain poorly understood. Here, we identified CD14, the major co-receptor for lipopolysaccharide detection, on dendritic cells as a previously undescribed binding partner of FimH, the protein located at the tip of the type 1 pilus of Escherichia coli. The FimH amino acids involved in CD14 binding are highly conserved across pathogenic and non-pathogenic strains. Binding of pathogenic bacteria to CD14 lead to reduced dendritic cell migration and blunted expression of co-stimulatory molecules, both rate-limiting factors of T cell activation. While defining an active molecular mechanism of immune evasion by pathogens, the interaction between FimH and CD14 represents a potential target to interfere with persistent and recurrent infections, such as urinary tract infections or Crohn’s disease. acknowledged_ssus: - _id: Bio - _id: PreCl - _id: EM-Fac acknowledgement: We thank Ulrich Dobrindt for providing UPEC strain CFT073, Vlad Gavra and Maximilian Götz, Bor Kavčič, Jonna Alanko and Eva Kiermaier for help with experiments and Robert Hauschild, Julian Stopp and Saren Tasciyan for help with data analysis. We thank the IST Austria Scientific Service Units, especially the Bioimaging facility, the Preclinical facility and the Electron microscopy facility for technical support, Jakob Wallner and all members of the Guet and Sixt lab for fruitful discussions and Daria Siekhaus for critically reading the manuscript. This work was supported by grants from the Austrian Research Promotion Agency (FEMtech 868984) to I.G., the European Research Council (CoG 724373) and the Austrian Science Fund (FWF P29911) to M.S. article_processing_charge: No author: - first_name: Kathrin full_name: Tomasek, Kathrin id: 3AEC8556-F248-11E8-B48F-1D18A9856A87 last_name: Tomasek orcid: 0000-0003-3768-877X - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Ivana full_name: Glatzová, Ivana id: 727b3c7d-4939-11ec-89b3-b9b0750ab74d last_name: Glatzová - first_name: Michael S. full_name: Lukesch, Michael S. last_name: Lukesch - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-4561-241X citation: ama: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. bioRxiv. doi:10.1101/2021.10.18.464770 apa: Tomasek, K., Leithner, A. F., Glatzová, I., Lukesch, M. S., Guet, C. C., & Sixt, M. K. (n.d.). Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. bioRxiv. Cold Spring Harbor Laboratory. https://doi.org/10.1101/2021.10.18.464770 chicago: Tomasek, Kathrin, Alexander F Leithner, Ivana Glatzová, Michael S. Lukesch, Calin C Guet, and Michael K Sixt. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack the Host Immune Response by Binding to CD14.” BioRxiv. Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2021.10.18.464770. ieee: K. Tomasek, A. F. Leithner, I. Glatzová, M. S. Lukesch, C. C. Guet, and M. K. Sixt, “Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14,” bioRxiv. Cold Spring Harbor Laboratory. ista: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. bioRxiv, 10.1101/2021.10.18.464770. mla: Tomasek, Kathrin, et al. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack the Host Immune Response by Binding to CD14.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2021.10.18.464770. short: K. Tomasek, A.F. Leithner, I. Glatzová, M.S. Lukesch, C.C. Guet, M.K. Sixt, BioRxiv (n.d.). date_created: 2021-11-19T12:24:16Z date_published: 2021-10-18T00:00:00Z date_updated: 2024-03-27T23:30:35Z day: '18' department: - _id: CaGu - _id: MiSi doi: 10.1101/2021.10.18.464770 ec_funded: 1 language: - iso: eng main_file_link: - open_access: '1' url: https://www.biorxiv.org/content/10.1101/2021.10.18.464770v1 month: '10' oa: 1 oa_version: Preprint project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 26018E70-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29911 name: Mechanical adaptation of lamellipodial actin publication: bioRxiv publication_status: submitted publisher: Cold Spring Harbor Laboratory related_material: record: - id: '11843' relation: later_version status: public - id: '10307' relation: dissertation_contains status: public status: public title: Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14 type: preprint user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9 year: '2021' ... --- _id: '7234' abstract: - lang: eng text: T lymphocytes utilize amoeboid migration to navigate effectively within complex microenvironments. The precise rearrangement of the actin cytoskeleton required for cellular forward propulsion is mediated by actin regulators, including the actin‐related protein 2/3 (Arp2/3) complex, a macromolecular machine that nucleates branched actin filaments at the leading edge. The consequences of modulating Arp2/3 activity on the biophysical properties of the actomyosin cortex and downstream T cell function are incompletely understood. We report that even a moderate decrease of Arp3 levels in T cells profoundly affects actin cortex integrity. Reduction in total F‐actin content leads to reduced cortical tension and disrupted lamellipodia formation. Instead, in Arp3‐knockdown cells, the motility mode is dominated by blebbing migration characterized by transient, balloon‐like protrusions at the leading edge. Although this migration mode seems to be compatible with interstitial migration in three‐dimensional environments, diminished locomotion kinetics and impaired cytotoxicity interfere with optimal T cell function. These findings define the importance of finely tuned, Arp2/3‐dependent mechanophysical membrane integrity in cytotoxic effector T lymphocyte activities. article_processing_charge: No article_type: original author: - first_name: Peyman full_name: Obeidy, Peyman last_name: Obeidy - first_name: Lining A. full_name: Ju, Lining A. last_name: Ju - first_name: Stefan H. full_name: Oehlers, Stefan H. last_name: Oehlers - first_name: Nursafwana S. full_name: Zulkhernain, Nursafwana S. last_name: Zulkhernain - first_name: Quintin full_name: Lee, Quintin last_name: Lee - first_name: Jorge L. full_name: Galeano Niño, Jorge L. last_name: Galeano Niño - first_name: Rain Y.Q. full_name: Kwan, Rain Y.Q. last_name: Kwan - first_name: Shweta full_name: Tikoo, Shweta last_name: Tikoo - first_name: Lois L. full_name: Cavanagh, Lois L. last_name: Cavanagh - first_name: Paulus full_name: Mrass, Paulus last_name: Mrass - first_name: Adam J.L. full_name: Cook, Adam J.L. last_name: Cook - first_name: Shaun P. full_name: Jackson, Shaun P. last_name: Jackson - first_name: Maté full_name: Biro, Maté last_name: Biro - first_name: Ben full_name: Roediger, Ben last_name: Roediger - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Wolfgang full_name: Weninger, Wolfgang last_name: Weninger citation: ama: Obeidy P, Ju LA, Oehlers SH, et al. Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes. Immunology and Cell Biology. 2020;98(2):93-113. doi:10.1111/imcb.12304 apa: Obeidy, P., Ju, L. A., Oehlers, S. H., Zulkhernain, N. S., Lee, Q., Galeano Niño, J. L., … Weninger, W. (2020). Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes. Immunology and Cell Biology. Wiley. https://doi.org/10.1111/imcb.12304 chicago: Obeidy, Peyman, Lining A. Ju, Stefan H. Oehlers, Nursafwana S. Zulkhernain, Quintin Lee, Jorge L. Galeano Niño, Rain Y.Q. Kwan, et al. “Partial Loss of Actin Nucleator Actin-Related Protein 2/3 Activity Triggers Blebbing in Primary T Lymphocytes.” Immunology and Cell Biology. Wiley, 2020. https://doi.org/10.1111/imcb.12304. ieee: P. Obeidy et al., “Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes,” Immunology and Cell Biology, vol. 98, no. 2. Wiley, pp. 93–113, 2020. ista: Obeidy P, Ju LA, Oehlers SH, Zulkhernain NS, Lee Q, Galeano Niño JL, Kwan RYQ, Tikoo S, Cavanagh LL, Mrass P, Cook AJL, Jackson SP, Biro M, Roediger B, Sixt MK, Weninger W. 2020. Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes. Immunology and Cell Biology. 98(2), 93–113. mla: Obeidy, Peyman, et al. “Partial Loss of Actin Nucleator Actin-Related Protein 2/3 Activity Triggers Blebbing in Primary T Lymphocytes.” Immunology and Cell Biology, vol. 98, no. 2, Wiley, 2020, pp. 93–113, doi:10.1111/imcb.12304. short: P. Obeidy, L.A. Ju, S.H. Oehlers, N.S. Zulkhernain, Q. Lee, J.L. Galeano Niño, R.Y.Q. Kwan, S. Tikoo, L.L. Cavanagh, P. Mrass, A.J.L. Cook, S.P. Jackson, M. Biro, B. Roediger, M.K. Sixt, W. Weninger, Immunology and Cell Biology 98 (2020) 93–113. date_created: 2020-01-05T23:00:48Z date_published: 2020-02-01T00:00:00Z date_updated: 2023-08-17T14:21:12Z day: '01' ddc: - '570' department: - _id: MiSi doi: 10.1111/imcb.12304 external_id: isi: - '000503885600001' pmid: - '31698518' file: - access_level: open_access checksum: c389477b4b52172ef76afff8a06c6775 content_type: application/pdf creator: dernst date_created: 2020-11-19T11:22:33Z date_updated: 2020-11-19T11:22:33Z file_id: '8775' file_name: 2020_ImmunologyCellBio_Obeidy.pdf file_size: 8569945 relation: main_file success: 1 file_date_updated: 2020-11-19T11:22:33Z has_accepted_license: '1' intvolume: ' 98' isi: 1 issue: '2' language: - iso: eng month: '02' oa: 1 oa_version: Published Version page: 93-113 pmid: 1 publication: Immunology and Cell Biology publication_identifier: eissn: - '14401711' issn: - '08189641' publication_status: published publisher: Wiley quality_controlled: '1' scopus_import: '1' status: public title: Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 98 year: '2020' ... --- _id: '7623' abstract: - lang: eng text: A two-dimensional mathematical model for cells migrating without adhesion capabilities is presented and analyzed. Cells are represented by their cortex, which is modeled as an elastic curve, subject to an internal pressure force. Net polymerization or depolymerization in the cortex is modeled via local addition or removal of material, driving a cortical flow. The model takes the form of a fully nonlinear degenerate parabolic system. An existence analysis is carried out by adapting ideas from the theory of gradient flows. Numerical simulations show that these simple rules can account for the behavior observed in experiments, suggesting a possible mechanical mechanism for adhesion-independent motility. acknowledgement: This work has been supported by the Vienna Science and Technology Fund, Grant no. LS13-029. G.J. and C.S. also acknowledge support by the Austrian Science Fund, Grants no. W1245, F 65, and W1261, as well as by the Fondation Sciences Mathématiques de Paris, and by Paris-Sciences-et-Lettres. article_processing_charge: No article_type: original author: - first_name: Gaspard full_name: Jankowiak, Gaspard last_name: Jankowiak - first_name: Diane full_name: Peurichard, Diane last_name: Peurichard - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Christian full_name: Schmeiser, Christian last_name: Schmeiser - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Jankowiak G, Peurichard D, Reversat A, Schmeiser C, Sixt MK. Modeling adhesion-independent cell migration. Mathematical Models and Methods in Applied Sciences. 2020;30(3):513-537. doi:10.1142/S021820252050013X apa: Jankowiak, G., Peurichard, D., Reversat, A., Schmeiser, C., & Sixt, M. K. (2020). Modeling adhesion-independent cell migration. Mathematical Models and Methods in Applied Sciences. World Scientific. https://doi.org/10.1142/S021820252050013X chicago: Jankowiak, Gaspard, Diane Peurichard, Anne Reversat, Christian Schmeiser, and Michael K Sixt. “Modeling Adhesion-Independent Cell Migration.” Mathematical Models and Methods in Applied Sciences. World Scientific, 2020. https://doi.org/10.1142/S021820252050013X. ieee: G. Jankowiak, D. Peurichard, A. Reversat, C. Schmeiser, and M. K. Sixt, “Modeling adhesion-independent cell migration,” Mathematical Models and Methods in Applied Sciences, vol. 30, no. 3. World Scientific, pp. 513–537, 2020. ista: Jankowiak G, Peurichard D, Reversat A, Schmeiser C, Sixt MK. 2020. Modeling adhesion-independent cell migration. Mathematical Models and Methods in Applied Sciences. 30(3), 513–537. mla: Jankowiak, Gaspard, et al. “Modeling Adhesion-Independent Cell Migration.” Mathematical Models and Methods in Applied Sciences, vol. 30, no. 3, World Scientific, 2020, pp. 513–37, doi:10.1142/S021820252050013X. short: G. Jankowiak, D. Peurichard, A. Reversat, C. Schmeiser, M.K. Sixt, Mathematical Models and Methods in Applied Sciences 30 (2020) 513–537. date_created: 2020-03-31T11:25:05Z date_published: 2020-03-18T00:00:00Z date_updated: 2023-08-18T10:18:56Z day: '18' department: - _id: MiSi doi: 10.1142/S021820252050013X external_id: arxiv: - '1903.09426' isi: - '000525349900003' intvolume: ' 30' isi: 1 issue: '3' language: - iso: eng main_file_link: - open_access: '1' url: https://arxiv.org/abs/1903.09426 month: '03' oa: 1 oa_version: Preprint page: 513-537 project: - _id: 25AD6156-B435-11E9-9278-68D0E5697425 grant_number: LS13-029 name: Modeling of Polarization and Motility of Leukocytes in Three-Dimensional Environments publication: Mathematical Models and Methods in Applied Sciences publication_identifier: issn: - '02182025' publication_status: published publisher: World Scientific quality_controlled: '1' scopus_import: '1' status: public title: Modeling adhesion-independent cell migration type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 30 year: '2020' ... --- _id: '7875' abstract: - lang: eng text: 'Cells navigating through complex tissues face a fundamental challenge: while multiple protrusions explore different paths, the cell needs to avoid entanglement. How a cell surveys and then corrects its own shape is poorly understood. Here, we demonstrate that spatially distinct microtubule dynamics regulate amoeboid cell migration by locally promoting the retraction of protrusions. In migrating dendritic cells, local microtubule depolymerization within protrusions remote from the microtubule organizing center triggers actomyosin contractility controlled by RhoA and its exchange factor Lfc. Depletion of Lfc leads to aberrant myosin localization, thereby causing two effects that rate-limit locomotion: (1) impaired cell edge coordination during path finding and (2) defective adhesion resolution. Compromised shape control is particularly hindering in geometrically complex microenvironments, where it leads to entanglement and ultimately fragmentation of the cell body. We thus demonstrate that microtubules can act as a proprioceptive device: they sense cell shape and control actomyosin retraction to sustain cellular coherence.' acknowledged_ssus: - _id: LifeSc - _id: Bio - _id: PreCl acknowledgement: "The authors thank the Scientific Service Units (Life Sciences, Bioimaging, Preclinical) of the Institute of Science and Technology Austria for excellent support. This work was funded by the European Research Council (ERC StG 281556 and CoG 724373), two grants from the Austrian\r\nScience Fund (FWF; P29911 and DK Nanocell W1250-B20 to M. Sixt) and by the German Research Foundation (DFG SFB1032 project B09) to O. Thorn-Seshold and D. Trauner. J. Renkawitz was supported by ISTFELLOW funding from the People Program (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) under the Research Executive Agency grant agreement (291734) and a European Molecular Biology Organization long-term fellowship (ALTF 1396-2014) co-funded by the European Commission (LTFCOFUND2013, GA-2013-609409), E. Kiermaier by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany’s Excellence Strategy—EXC 2151—390873048, and H. Hacker by the American Lebanese Syrian Associated ¨Charities. K.-D. Fischer was supported by the Analysis, Imaging and Modelling of Neuronal and Inflammatory Processes graduate school funded by the Ministry of Economics, Science, and Digitisation of the State Saxony-Anhalt and by the European Funds for Social and Regional Development." article_number: e201907154 article_processing_charge: No article_type: original author: - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Irute full_name: Girkontaite, Irute last_name: Girkontaite - first_name: Kerry full_name: Tedford, Kerry last_name: Tedford - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Oliver full_name: Thorn-Seshold, Oliver last_name: Thorn-Seshold - first_name: Dirk full_name: Trauner, Dirk id: E8F27F48-3EBA-11E9-92A1-B709E6697425 last_name: Trauner - first_name: Hans full_name: Häcker, Hans last_name: Häcker - first_name: Klaus Dieter full_name: Fischer, Klaus Dieter last_name: Fischer - first_name: Eva full_name: Kiermaier, Eva id: 3EB04B78-F248-11E8-B48F-1D18A9856A87 last_name: Kiermaier orcid: 0000-0001-6165-5738 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Kopf A, Renkawitz J, Hauschild R, et al. Microtubules control cellular shape and coherence in amoeboid migrating cells. The Journal of Cell Biology. 2020;219(6). doi:10.1083/jcb.201907154 apa: Kopf, A., Renkawitz, J., Hauschild, R., Girkontaite, I., Tedford, K., Merrin, J., … Sixt, M. K. (2020). Microtubules control cellular shape and coherence in amoeboid migrating cells. The Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201907154 chicago: Kopf, Aglaja, Jörg Renkawitz, Robert Hauschild, Irute Girkontaite, Kerry Tedford, Jack Merrin, Oliver Thorn-Seshold, et al. “Microtubules Control Cellular Shape and Coherence in Amoeboid Migrating Cells.” The Journal of Cell Biology. Rockefeller University Press, 2020. https://doi.org/10.1083/jcb.201907154. ieee: A. Kopf et al., “Microtubules control cellular shape and coherence in amoeboid migrating cells,” The Journal of Cell Biology, vol. 219, no. 6. Rockefeller University Press, 2020. ista: Kopf A, Renkawitz J, Hauschild R, Girkontaite I, Tedford K, Merrin J, Thorn-Seshold O, Trauner D, Häcker H, Fischer KD, Kiermaier E, Sixt MK. 2020. Microtubules control cellular shape and coherence in amoeboid migrating cells. The Journal of Cell Biology. 219(6), e201907154. mla: Kopf, Aglaja, et al. “Microtubules Control Cellular Shape and Coherence in Amoeboid Migrating Cells.” The Journal of Cell Biology, vol. 219, no. 6, e201907154, Rockefeller University Press, 2020, doi:10.1083/jcb.201907154. short: A. Kopf, J. Renkawitz, R. Hauschild, I. Girkontaite, K. Tedford, J. Merrin, O. Thorn-Seshold, D. Trauner, H. Häcker, K.D. Fischer, E. Kiermaier, M.K. Sixt, The Journal of Cell Biology 219 (2020). date_created: 2020-05-24T22:00:56Z date_published: 2020-06-01T00:00:00Z date_updated: 2023-08-21T06:28:17Z day: '01' ddc: - '570' department: - _id: MiSi - _id: Bio - _id: NanoFab doi: 10.1083/jcb.201907154 ec_funded: 1 external_id: isi: - '000538141100020' pmid: - '32379884' file: - access_level: open_access checksum: cb0b9c77842ae1214caade7b77e4d82d content_type: application/pdf creator: dernst date_created: 2020-11-24T13:25:13Z date_updated: 2020-11-24T13:25:13Z file_id: '8801' file_name: 2020_JCellBiol_Kopf.pdf file_size: 7536712 relation: main_file success: 1 file_date_updated: 2020-11-24T13:25:13Z has_accepted_license: '1' intvolume: ' 219' isi: 1 issue: '6' language: - iso: eng month: '06' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 26018E70-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29911 name: Mechanical adaptation of lamellipodial actin - _id: 252C3B08-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: W 1250-B20 name: Nano-Analytics of Cellular Systems - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme - _id: 25A48D24-B435-11E9-9278-68D0E5697425 grant_number: ALTF 1396-2014 name: Molecular and system level view of immune cell migration publication: The Journal of Cell Biology publication_identifier: eissn: - 1540-8140 publication_status: published publisher: Rockefeller University Press quality_controlled: '1' scopus_import: '1' status: public title: Microtubules control cellular shape and coherence in amoeboid migrating cells tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 219 year: '2020' ... --- _id: '7876' abstract: - lang: eng text: 'In contrast to lymph nodes, the lymphoid regions of the spleen—the white pulp—are located deep within the organ, yielding the trafficking paths of T cells in the white pulp largely invisible. In an intravital microscopy tour de force reported in this issue of Immunity, Chauveau et al. show that T cells perform unidirectional, perivascular migration through the enigmatic marginal zone bridging channels. ' article_processing_charge: No article_type: original author: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Tim full_name: Lämmermann, Tim last_name: Lämmermann citation: ama: 'Sixt MK, Lämmermann T. T cells: Bridge-and-channel commute to the white pulp. Immunity. 2020;52(5):721-723. doi:10.1016/j.immuni.2020.04.020' apa: 'Sixt, M. K., & Lämmermann, T. (2020). T cells: Bridge-and-channel commute to the white pulp. Immunity. Elsevier. https://doi.org/10.1016/j.immuni.2020.04.020' chicago: 'Sixt, Michael K, and Tim Lämmermann. “T Cells: Bridge-and-Channel Commute to the White Pulp.” Immunity. Elsevier, 2020. https://doi.org/10.1016/j.immuni.2020.04.020.' ieee: 'M. K. Sixt and T. Lämmermann, “T cells: Bridge-and-channel commute to the white pulp,” Immunity, vol. 52, no. 5. Elsevier, pp. 721–723, 2020.' ista: 'Sixt MK, Lämmermann T. 2020. T cells: Bridge-and-channel commute to the white pulp. Immunity. 52(5), 721–723.' mla: 'Sixt, Michael K., and Tim Lämmermann. “T Cells: Bridge-and-Channel Commute to the White Pulp.” Immunity, vol. 52, no. 5, Elsevier, 2020, pp. 721–23, doi:10.1016/j.immuni.2020.04.020.' short: M.K. Sixt, T. Lämmermann, Immunity 52 (2020) 721–723. date_created: 2020-05-24T22:00:57Z date_published: 2020-05-19T00:00:00Z date_updated: 2023-08-21T06:27:18Z day: '19' department: - _id: MiSi doi: 10.1016/j.immuni.2020.04.020 external_id: isi: - '000535371100002' intvolume: ' 52' isi: 1 issue: '5' language: - iso: eng main_file_link: - open_access: '1' url: https://pure.mpg.de/pubman/item/item_3265599_2/component/file_3265620/Sixt%20et%20al..pdf month: '05' oa: 1 oa_version: Published Version page: 721-723 publication: Immunity publication_identifier: eissn: - '10974180' issn: - '10747613' publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: 'T cells: Bridge-and-channel commute to the white pulp' type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 52 year: '2020' ... --- _id: '7909' abstract: - lang: eng text: Cell migration entails networks and bundles of actin filaments termed lamellipodia and microspikes or filopodia, respectively, as well as focal adhesions, all of which recruit Ena/VASP family members hitherto thought to antagonize efficient cell motility. However, we find these proteins to act as positive regulators of migration in different murine cell lines. CRISPR/Cas9-mediated loss of Ena/VASP proteins reduced lamellipodial actin assembly and perturbed lamellipodial architecture, as evidenced by changed network geometry as well as reduction of filament length and number that was accompanied by abnormal Arp2/3 complex and heterodimeric capping protein accumulation. Loss of Ena/VASP function also abolished the formation of microspikes normally embedded in lamellipodia, but not of filopodia capable of emanating without lamellipodia. Ena/VASP-deficiency also impaired integrin-mediated adhesion accompanied by reduced traction forces exerted through these structures. Our data thus uncover novel Ena/VASP functions of these actin polymerases that are fully consistent with their promotion of cell migration. article_number: e55351 article_processing_charge: No article_type: original author: - first_name: Julia full_name: Damiano-Guercio, Julia last_name: Damiano-Guercio - first_name: Laëtitia full_name: Kurzawa, Laëtitia last_name: Kurzawa - first_name: Jan full_name: Müller, Jan id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D last_name: Müller - first_name: Georgi A full_name: Dimchev, Georgi A id: 38C393BE-F248-11E8-B48F-1D18A9856A87 last_name: Dimchev orcid: 0000-0001-8370-6161 - first_name: Matthias full_name: Schaks, Matthias last_name: Schaks - first_name: Maria full_name: Nemethova, Maria id: 34E27F1C-F248-11E8-B48F-1D18A9856A87 last_name: Nemethova - first_name: Thomas full_name: Pokrant, Thomas last_name: Pokrant - first_name: Stefan full_name: Brühmann, Stefan last_name: Brühmann - first_name: Joern full_name: Linkner, Joern last_name: Linkner - first_name: Laurent full_name: Blanchoin, Laurent last_name: Blanchoin - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner - first_name: Jan full_name: Faix, Jan last_name: Faix citation: ama: Damiano-Guercio J, Kurzawa L, Müller J, et al. Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion. eLife. 2020;9. doi:10.7554/eLife.55351 apa: Damiano-Guercio, J., Kurzawa, L., Müller, J., Dimchev, G. A., Schaks, M., Nemethova, M., … Faix, J. (2020). Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.55351 chicago: Damiano-Guercio, Julia, Laëtitia Kurzawa, Jan Müller, Georgi A Dimchev, Matthias Schaks, Maria Nemethova, Thomas Pokrant, et al. “Loss of Ena/VASP Interferes with Lamellipodium Architecture, Motility and Integrin-Dependent Adhesion.” ELife. eLife Sciences Publications, 2020. https://doi.org/10.7554/eLife.55351. ieee: J. Damiano-Guercio et al., “Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion,” eLife, vol. 9. eLife Sciences Publications, 2020. ista: Damiano-Guercio J, Kurzawa L, Müller J, Dimchev GA, Schaks M, Nemethova M, Pokrant T, Brühmann S, Linkner J, Blanchoin L, Sixt MK, Rottner K, Faix J. 2020. Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion. eLife. 9, e55351. mla: Damiano-Guercio, Julia, et al. “Loss of Ena/VASP Interferes with Lamellipodium Architecture, Motility and Integrin-Dependent Adhesion.” ELife, vol. 9, e55351, eLife Sciences Publications, 2020, doi:10.7554/eLife.55351. short: J. Damiano-Guercio, L. Kurzawa, J. Müller, G.A. Dimchev, M. Schaks, M. Nemethova, T. Pokrant, S. Brühmann, J. Linkner, L. Blanchoin, M.K. Sixt, K. Rottner, J. Faix, ELife 9 (2020). date_created: 2020-05-31T22:00:49Z date_published: 2020-05-11T00:00:00Z date_updated: 2023-08-21T06:32:25Z day: '11' ddc: - '570' department: - _id: MiSi doi: 10.7554/eLife.55351 ec_funded: 1 external_id: isi: - '000537208000001' file: - access_level: open_access checksum: d33bd4441b9a0195718ce1ba5d2c48a6 content_type: application/pdf creator: dernst date_created: 2020-06-02T10:35:37Z date_updated: 2020-07-14T12:48:05Z file_id: '7914' file_name: 2020_eLife_Damiano_Guercio.pdf file_size: 10535713 relation: main_file file_date_updated: 2020-07-14T12:48:05Z has_accepted_license: '1' intvolume: ' 9' isi: 1 language: - iso: eng month: '05' oa: 1 oa_version: Published Version project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: eLife publication_identifier: eissn: - 2050084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 9 year: '2020' ... --- _id: '8132' abstract: - lang: eng text: The WAVE regulatory complex (WRC) is crucial for assembly of the peripheral branched actin network constituting one of the main drivers of eukaryotic cell migration. Here, we uncover an essential role of the hematopoietic-specific WRC component HEM1 for immune cell development. Germline-encoded HEM1 deficiency underlies an inborn error of immunity with systemic autoimmunity, at cellular level marked by WRC destabilization, reduced filamentous actin, and failure to assemble lamellipodia. Hem1−/− mice display systemic autoimmunity, phenocopying the human disease. In the absence of Hem1, B cells become deprived of extracellular stimuli necessary to maintain the strength of B cell receptor signaling at a level permissive for survival of non-autoreactive B cells. This shifts the balance of B cell fate choices toward autoreactive B cells and thus autoimmunity. article_number: eabc3979 article_processing_charge: No article_type: original author: - first_name: Elisabeth full_name: Salzer, Elisabeth last_name: Salzer - first_name: Samaneh full_name: Zoghi, Samaneh last_name: Zoghi - first_name: Máté G. full_name: Kiss, Máté G. last_name: Kiss - first_name: Frieda full_name: Kage, Frieda last_name: Kage - first_name: Christina full_name: Rashkova, Christina last_name: Rashkova - first_name: Stephanie full_name: Stahnke, Stephanie last_name: Stahnke - first_name: Matthias full_name: Haimel, Matthias last_name: Haimel - first_name: René full_name: Platzer, René last_name: Platzer - first_name: Michael full_name: Caldera, Michael last_name: Caldera - first_name: Rico Chandra full_name: Ardy, Rico Chandra last_name: Ardy - first_name: Birgit full_name: Hoeger, Birgit last_name: Hoeger - first_name: Jana full_name: Block, Jana last_name: Block - first_name: David full_name: Medgyesi, David last_name: Medgyesi - first_name: Celine full_name: Sin, Celine last_name: Sin - first_name: Sepideh full_name: Shahkarami, Sepideh last_name: Shahkarami - first_name: Renate full_name: Kain, Renate last_name: Kain - first_name: Vahid full_name: Ziaee, Vahid last_name: Ziaee - first_name: Peter full_name: Hammerl, Peter last_name: Hammerl - first_name: Christoph full_name: Bock, Christoph last_name: Bock - first_name: Jörg full_name: Menche, Jörg last_name: Menche - first_name: Loïc full_name: Dupré, Loïc last_name: Dupré - first_name: Johannes B. full_name: Huppa, Johannes B. last_name: Huppa - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Alexis full_name: Lomakin, Alexis last_name: Lomakin - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner - first_name: Christoph J. full_name: Binder, Christoph J. last_name: Binder - first_name: Theresia E.B. full_name: Stradal, Theresia E.B. last_name: Stradal - first_name: Nima full_name: Rezaei, Nima last_name: Rezaei - first_name: Kaan full_name: Boztug, Kaan last_name: Boztug citation: ama: Salzer E, Zoghi S, Kiss MG, et al. The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity. Science Immunology. 2020;5(49). doi:10.1126/sciimmunol.abc3979 apa: Salzer, E., Zoghi, S., Kiss, M. G., Kage, F., Rashkova, C., Stahnke, S., … Boztug, K. (2020). The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity. Science Immunology. AAAS. https://doi.org/10.1126/sciimmunol.abc3979 chicago: Salzer, Elisabeth, Samaneh Zoghi, Máté G. Kiss, Frieda Kage, Christina Rashkova, Stephanie Stahnke, Matthias Haimel, et al. “The Cytoskeletal Regulator HEM1 Governs B Cell Development and Prevents Autoimmunity.” Science Immunology. AAAS, 2020. https://doi.org/10.1126/sciimmunol.abc3979. ieee: E. Salzer et al., “The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity,” Science Immunology, vol. 5, no. 49. AAAS, 2020. ista: Salzer E, Zoghi S, Kiss MG, Kage F, Rashkova C, Stahnke S, Haimel M, Platzer R, Caldera M, Ardy RC, Hoeger B, Block J, Medgyesi D, Sin C, Shahkarami S, Kain R, Ziaee V, Hammerl P, Bock C, Menche J, Dupré L, Huppa JB, Sixt MK, Lomakin A, Rottner K, Binder CJ, Stradal TEB, Rezaei N, Boztug K. 2020. The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity. Science Immunology. 5(49), eabc3979. mla: Salzer, Elisabeth, et al. “The Cytoskeletal Regulator HEM1 Governs B Cell Development and Prevents Autoimmunity.” Science Immunology, vol. 5, no. 49, eabc3979, AAAS, 2020, doi:10.1126/sciimmunol.abc3979. short: E. Salzer, S. Zoghi, M.G. Kiss, F. Kage, C. Rashkova, S. Stahnke, M. Haimel, R. Platzer, M. Caldera, R.C. Ardy, B. Hoeger, J. Block, D. Medgyesi, C. Sin, S. Shahkarami, R. Kain, V. Ziaee, P. Hammerl, C. Bock, J. Menche, L. Dupré, J.B. Huppa, M.K. Sixt, A. Lomakin, K. Rottner, C.J. Binder, T.E.B. Stradal, N. Rezaei, K. Boztug, Science Immunology 5 (2020). date_created: 2020-07-19T22:00:58Z date_published: 2020-07-10T00:00:00Z date_updated: 2023-08-22T07:56:04Z day: '10' department: - _id: MiSi doi: 10.1126/sciimmunol.abc3979 external_id: isi: - '000546994600004' pmid: - '32646852' intvolume: ' 5' isi: 1 issue: '49' language: - iso: eng month: '07' oa_version: None pmid: 1 publication: Science Immunology publication_identifier: eissn: - '24709468' publication_status: published publisher: AAAS quality_controlled: '1' scopus_import: '1' status: public title: The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 5 year: '2020' ... --- _id: '8787' abstract: - lang: eng text: Breakdown of vascular barriers is a major complication of inflammatory diseases. Anucleate platelets form blood-clots during thrombosis, but also play a crucial role in inflammation. While spatio-temporal dynamics of clot formation are well characterized, the cell-biological mechanisms of platelet recruitment to inflammatory micro-environments remain incompletely understood. Here we identify Arp2/3-dependent lamellipodia formation as a prominent morphological feature of immune-responsive platelets. Platelets use lamellipodia to scan for fibrin(ogen) deposited on the inflamed vasculature and to directionally spread, to polarize and to govern haptotactic migration along gradients of the adhesive ligand. Platelet-specific abrogation of Arp2/3 interferes with haptotactic repositioning of platelets to microlesions, thus impairing vascular sealing and provoking inflammatory microbleeding. During infection, haptotaxis promotes capture of bacteria and prevents hematogenic dissemination, rendering platelets gate-keepers of the inflamed microvasculature. Consequently, these findings identify haptotaxis as a key effector function of immune-responsive platelets. acknowledgement: "We thank Sebastian Helmer, Nicole Blount, Christine Mann, and Beate Jantz for technical assistance; Hellen Ishikawa-Ankerhold for help and advice; Michael Sixt for critical\r\ndiscussions. This study was supported by the DFG SFB 914 (S.M. [B02 and Z01], K.Sch.\r\n[B02], B.W. [A02 and Z03], C.A.R. [B03], C.S. [A10], J.P. [Gerok position]), the DFG\r\nSFB 1123 (S.M. [B06]), the DFG FOR 2033 (S.M. and F.G.), the German Center for\r\nCardiovascular Research (DZHK) (Clinician Scientist Program [L.N.], MHA 1.4VD\r\n[S.M.], Postdoc Start-up Grant, 81×3600213 [F.G.]), FP7 program (project 260309,\r\nPRESTIGE [S.M.]), FöFoLe project 1015/1009 (L.N.), FöFoLe project 947 (F.G.), the\r\nFriedrich-Baur-Stiftung project 41/16 (F.G.), and LMUexcellence NFF (F.G.). This project has received funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program (grant agreement no.\r\n833440) (S.M.). F.G. received funding from the European Union’s Horizon 2020 research\r\nand innovation program under the Marie Skłodowska-Curie grant agreement no.\r\n747687." article_number: '5778' article_processing_charge: No article_type: original author: - first_name: Leo full_name: Nicolai, Leo last_name: Nicolai - first_name: Karin full_name: Schiefelbein, Karin last_name: Schiefelbein - first_name: Silvia full_name: Lipsky, Silvia last_name: Lipsky - first_name: Alexander full_name: Leunig, Alexander last_name: Leunig - first_name: Marie full_name: Hoffknecht, Marie last_name: Hoffknecht - first_name: Kami full_name: Pekayvaz, Kami last_name: Pekayvaz - first_name: Ben full_name: Raude, Ben last_name: Raude - first_name: Charlotte full_name: Marx, Charlotte last_name: Marx - first_name: Andreas full_name: Ehrlich, Andreas last_name: Ehrlich - first_name: Joachim full_name: Pircher, Joachim last_name: Pircher - first_name: Zhe full_name: Zhang, Zhe last_name: Zhang - first_name: Inas full_name: Saleh, Inas last_name: Saleh - first_name: Anna-Kristina full_name: Marel, Anna-Kristina last_name: Marel - first_name: Achim full_name: Löf, Achim last_name: Löf - first_name: Tobias full_name: Petzold, Tobias last_name: Petzold - first_name: Michael full_name: Lorenz, Michael last_name: Lorenz - first_name: Konstantin full_name: Stark, Konstantin last_name: Stark - first_name: Robert full_name: Pick, Robert last_name: Pick - first_name: Gerhild full_name: Rosenberger, Gerhild last_name: Rosenberger - first_name: Ludwig full_name: Weckbach, Ludwig last_name: Weckbach - first_name: Bernd full_name: Uhl, Bernd last_name: Uhl - first_name: Sheng full_name: Xia, Sheng last_name: Xia - first_name: Christoph Andreas full_name: Reichel, Christoph Andreas last_name: Reichel - first_name: Barbara full_name: Walzog, Barbara last_name: Walzog - first_name: Christian full_name: Schulz, Christian last_name: Schulz - first_name: Vanessa full_name: Zheden, Vanessa id: 39C5A68A-F248-11E8-B48F-1D18A9856A87 last_name: Zheden orcid: 0000-0002-9438-4783 - first_name: Markus full_name: Bender, Markus last_name: Bender - first_name: Rong full_name: Li, Rong last_name: Li - first_name: Steffen full_name: Massberg, Steffen last_name: Massberg - first_name: Florian R full_name: Gärtner, Florian R id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 citation: ama: Nicolai L, Schiefelbein K, Lipsky S, et al. Vascular surveillance by haptotactic blood platelets in inflammation and infection. Nature Communications. 2020;11. doi:10.1038/s41467-020-19515-0 apa: Nicolai, L., Schiefelbein, K., Lipsky, S., Leunig, A., Hoffknecht, M., Pekayvaz, K., … Gärtner, F. R. (2020). Vascular surveillance by haptotactic blood platelets in inflammation and infection. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-020-19515-0 chicago: Nicolai, Leo, Karin Schiefelbein, Silvia Lipsky, Alexander Leunig, Marie Hoffknecht, Kami Pekayvaz, Ben Raude, et al. “Vascular Surveillance by Haptotactic Blood Platelets in Inflammation and Infection.” Nature Communications. Springer Nature, 2020. https://doi.org/10.1038/s41467-020-19515-0. ieee: L. Nicolai et al., “Vascular surveillance by haptotactic blood platelets in inflammation and infection,” Nature Communications, vol. 11. Springer Nature, 2020. ista: Nicolai L, Schiefelbein K, Lipsky S, Leunig A, Hoffknecht M, Pekayvaz K, Raude B, Marx C, Ehrlich A, Pircher J, Zhang Z, Saleh I, Marel A-K, Löf A, Petzold T, Lorenz M, Stark K, Pick R, Rosenberger G, Weckbach L, Uhl B, Xia S, Reichel CA, Walzog B, Schulz C, Zheden V, Bender M, Li R, Massberg S, Gärtner FR. 2020. Vascular surveillance by haptotactic blood platelets in inflammation and infection. Nature Communications. 11, 5778. mla: Nicolai, Leo, et al. “Vascular Surveillance by Haptotactic Blood Platelets in Inflammation and Infection.” Nature Communications, vol. 11, 5778, Springer Nature, 2020, doi:10.1038/s41467-020-19515-0. short: L. Nicolai, K. Schiefelbein, S. Lipsky, A. Leunig, M. Hoffknecht, K. Pekayvaz, B. Raude, C. Marx, A. Ehrlich, J. Pircher, Z. Zhang, I. Saleh, A.-K. Marel, A. Löf, T. Petzold, M. Lorenz, K. Stark, R. Pick, G. Rosenberger, L. Weckbach, B. Uhl, S. Xia, C.A. Reichel, B. Walzog, C. Schulz, V. Zheden, M. Bender, R. Li, S. Massberg, F.R. Gärtner, Nature Communications 11 (2020). date_created: 2020-11-22T23:01:23Z date_published: 2020-11-13T00:00:00Z date_updated: 2023-08-22T13:26:26Z day: '13' ddc: - '570' department: - _id: MiSi - _id: EM-Fac doi: 10.1038/s41467-020-19515-0 ec_funded: 1 external_id: isi: - '000594648000014' pmid: - '33188196' file: - access_level: open_access checksum: 485b7b6cf30198ba0ce126491a28f125 content_type: application/pdf creator: dernst date_created: 2020-11-23T13:29:49Z date_updated: 2020-11-23T13:29:49Z file_id: '8798' file_name: 2020_NatureComm_Nicolai.pdf file_size: 7035340 relation: main_file success: 1 file_date_updated: 2020-11-23T13:29:49Z has_accepted_license: '1' intvolume: ' 11' isi: 1 language: - iso: eng month: '11' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 260AA4E2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '747687' name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells publication: Nature Communications publication_identifier: eissn: - '20411723' publication_status: published publisher: Springer Nature quality_controlled: '1' related_material: link: - relation: erratum url: https://doi.org/10.1038/s41467-022-31310-7 scopus_import: '1' status: public title: Vascular surveillance by haptotactic blood platelets in inflammation and infection tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 11 year: '2020' ... --- _id: '8142' abstract: - lang: eng text: Cell production and differentiation for the acquisition of specific functions are key features of living systems. The dynamic network of cellular microtubules provides the necessary platform to accommodate processes associated with the transition of cells through the individual phases of cytogenesis. Here, we show that the plant hormone cytokinin fine‐tunes the activity of the microtubular cytoskeleton during cell differentiation and counteracts microtubular rearrangements driven by the hormone auxin. The endogenous upward gradient of cytokinin activity along the longitudinal growth axis in Arabidopsis thaliana roots correlates with robust rearrangements of the microtubule cytoskeleton in epidermal cells progressing from the proliferative to the differentiation stage. Controlled increases in cytokinin activity result in premature re‐organization of the microtubule network from transversal to an oblique disposition in cells prior to their differentiation, whereas attenuated hormone perception delays cytoskeleton conversion into a configuration typical for differentiated cells. Intriguingly, cytokinin can interfere with microtubules also in animal cells, such as leukocytes, suggesting that a cytokinin‐sensitive control pathway for the microtubular cytoskeleton may be at least partially conserved between plant and animal cells. acknowledged_ssus: - _id: Bio - _id: LifeSc acknowledgement: We thank Takashi Aoyama, David Alabadi, and Bert De Rybel for sharing material, Jiří Friml, Maciek Adamowski, and Katerina Schwarzerová for inspiring discussions, and Martine De Cock for help in preparing the manuscript. This research was supported by the Scientific Service Units (SSUs) of IST Austria through resources provided by the Bioimaging Facility (BIF), especially to Robert Hauschild; and the Life Science Facility (LSF). J.C.M. is the recipient of a EMBO Long‐Term Fellowship (ALTF number 710‐2016). This work was supported with MEYS CR, project no.CZ.02.1.01/0.0/0.0/16_019/0000738 to J.P., and by the Austrian Science Fund (FWF01_I1774S) to E.B. article_number: e104238 article_processing_charge: Yes (via OA deal) article_type: original author: - first_name: Juan C full_name: Montesinos López, Juan C id: 310A8E3E-F248-11E8-B48F-1D18A9856A87 last_name: Montesinos López orcid: 0000-0001-9179-6099 - first_name: A full_name: Abuzeineh, A last_name: Abuzeineh - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Alba full_name: Juanes Garcia, Alba id: 40F05888-F248-11E8-B48F-1D18A9856A87 last_name: Juanes Garcia orcid: 0000-0002-1009-9652 - first_name: Krisztina full_name: Ötvös, Krisztina id: 29B901B0-F248-11E8-B48F-1D18A9856A87 last_name: Ötvös orcid: 0000-0002-5503-4983 - first_name: J full_name: Petrášek, J last_name: Petrášek - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Eva full_name: Benková, Eva id: 38F4F166-F248-11E8-B48F-1D18A9856A87 last_name: Benková orcid: 0000-0002-8510-9739 citation: ama: Montesinos López JC, Abuzeineh A, Kopf A, et al. Phytohormone cytokinin guides microtubule dynamics during cell progression from proliferative to differentiated stage. The Embo Journal. 2020;39(17). doi:10.15252/embj.2019104238 apa: Montesinos López, J. C., Abuzeineh, A., Kopf, A., Juanes Garcia, A., Ötvös, K., Petrášek, J., … Benková, E. (2020). Phytohormone cytokinin guides microtubule dynamics during cell progression from proliferative to differentiated stage. The Embo Journal. Embo Press. https://doi.org/10.15252/embj.2019104238 chicago: Montesinos López, Juan C, A Abuzeineh, Aglaja Kopf, Alba Juanes Garcia, Krisztina Ötvös, J Petrášek, Michael K Sixt, and Eva Benková. “Phytohormone Cytokinin Guides Microtubule Dynamics during Cell Progression from Proliferative to Differentiated Stage.” The Embo Journal. Embo Press, 2020. https://doi.org/10.15252/embj.2019104238. ieee: J. C. Montesinos López et al., “Phytohormone cytokinin guides microtubule dynamics during cell progression from proliferative to differentiated stage,” The Embo Journal, vol. 39, no. 17. Embo Press, 2020. ista: Montesinos López JC, Abuzeineh A, Kopf A, Juanes Garcia A, Ötvös K, Petrášek J, Sixt MK, Benková E. 2020. Phytohormone cytokinin guides microtubule dynamics during cell progression from proliferative to differentiated stage. The Embo Journal. 39(17), e104238. mla: Montesinos López, Juan C., et al. “Phytohormone Cytokinin Guides Microtubule Dynamics during Cell Progression from Proliferative to Differentiated Stage.” The Embo Journal, vol. 39, no. 17, e104238, Embo Press, 2020, doi:10.15252/embj.2019104238. short: J.C. Montesinos López, A. Abuzeineh, A. Kopf, A. Juanes Garcia, K. Ötvös, J. Petrášek, M.K. Sixt, E. Benková, The Embo Journal 39 (2020). date_created: 2020-07-21T09:08:38Z date_published: 2020-09-01T00:00:00Z date_updated: 2023-09-05T13:05:47Z day: '01' ddc: - '580' department: - _id: MiSi - _id: EvBe doi: 10.15252/embj.2019104238 external_id: isi: - '000548311800001' pmid: - '32667089' file: - access_level: open_access checksum: 43d2b36598708e6ab05c69074e191d57 content_type: application/pdf creator: dernst date_created: 2020-12-02T09:13:23Z date_updated: 2020-12-02T09:13:23Z file_id: '8827' file_name: 2020_EMBO_Montesinos.pdf file_size: 3497156 relation: main_file success: 1 file_date_updated: 2020-12-02T09:13:23Z has_accepted_license: '1' intvolume: ' 39' isi: 1 issue: '17' language: - iso: eng month: '09' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 253E54C8-B435-11E9-9278-68D0E5697425 grant_number: ALTF710-2016 name: Molecular mechanism of auxindriven formative divisions delineating lateral root organogenesis in plants - _id: 2542D156-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: I 1774-B16 name: Hormone cross-talk drives nutrient dependent plant development publication: The Embo Journal publication_identifier: eissn: - 1460-2075 issn: - 0261-4189 publication_status: published publisher: Embo Press quality_controlled: '1' scopus_import: '1' status: public title: Phytohormone cytokinin guides microtubule dynamics during cell progression from proliferative to differentiated stage tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 39 year: '2020' ... --- _id: '7885' abstract: - lang: eng text: Eukaryotic cells migrate by coupling the intracellular force of the actin cytoskeleton to the environment. While force coupling is usually mediated by transmembrane adhesion receptors, especially those of the integrin family, amoeboid cells such as leukocytes can migrate extremely fast despite very low adhesive forces1. Here we show that leukocytes cannot only migrate under low adhesion but can also transmit forces in the complete absence of transmembrane force coupling. When confined within three-dimensional environments, they use the topographical features of the substrate to propel themselves. Here the retrograde flow of the actin cytoskeleton follows the texture of the substrate, creating retrograde shear forces that are sufficient to drive the cell body forwards. Notably, adhesion-dependent and adhesion-independent migration are not mutually exclusive, but rather are variants of the same principle of coupling retrograde actin flow to the environment and thus can potentially operate interchangeably and simultaneously. As adhesion-free migration is independent of the chemical composition of the environment, it renders cells completely autonomous in their locomotive behaviour. acknowledged_ssus: - _id: Bio - _id: LifeSc - _id: M-Shop acknowledgement: We thank A. Leithner and J. Renkawitz for discussion and critical reading of the manuscript; J. Schwarz and M. Mehling for establishing the microfluidic setups; the Bioimaging Facility of IST Austria for excellent support, as well as the Life Science Facility and the Miba Machine Shop of IST Austria; and F. N. Arslan, L. E. Burnett and L. Li for their work during their rotation in the IST PhD programme. This work was supported by the European Research Council (ERC StG 281556 and CoG 724373) to M.S. and grants from the Austrian Science Fund (FWF P29911) and the WWTF to M.S. M.H. was supported by the European Regional Development Fund Project (CZ.02.1.01/0.0/0.0/15_003/0000476). F.G. received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 747687. article_processing_charge: No article_type: original author: - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Florian R full_name: Gärtner, Florian R id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Julian A full_name: Stopp, Julian A id: 489E3F00-F248-11E8-B48F-1D18A9856A87 last_name: Stopp - first_name: Saren full_name: Tasciyan, Saren id: 4323B49C-F248-11E8-B48F-1D18A9856A87 last_name: Tasciyan orcid: 0000-0003-1671-393X - first_name: Juan L full_name: Aguilera Servin, Juan L id: 2A67C376-F248-11E8-B48F-1D18A9856A87 last_name: Aguilera Servin orcid: 0000-0002-2862-8372 - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Matthieu full_name: Piel, Matthieu last_name: Piel - first_name: Andrew full_name: Callan-Jones, Andrew last_name: Callan-Jones - first_name: Raphael full_name: Voituriez, Raphael last_name: Voituriez - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Reversat A, Gärtner FR, Merrin J, et al. Cellular locomotion using environmental topography. Nature. 2020;582:582–585. doi:10.1038/s41586-020-2283-z apa: Reversat, A., Gärtner, F. R., Merrin, J., Stopp, J. A., Tasciyan, S., Aguilera Servin, J. L., … Sixt, M. K. (2020). Cellular locomotion using environmental topography. Nature. Springer Nature. https://doi.org/10.1038/s41586-020-2283-z chicago: Reversat, Anne, Florian R Gärtner, Jack Merrin, Julian A Stopp, Saren Tasciyan, Juan L Aguilera Servin, Ingrid de Vries, et al. “Cellular Locomotion Using Environmental Topography.” Nature. Springer Nature, 2020. https://doi.org/10.1038/s41586-020-2283-z. ieee: A. Reversat et al., “Cellular locomotion using environmental topography,” Nature, vol. 582. Springer Nature, pp. 582–585, 2020. ista: Reversat A, Gärtner FR, Merrin J, Stopp JA, Tasciyan S, Aguilera Servin JL, de Vries I, Hauschild R, Hons M, Piel M, Callan-Jones A, Voituriez R, Sixt MK. 2020. Cellular locomotion using environmental topography. Nature. 582, 582–585. mla: Reversat, Anne, et al. “Cellular Locomotion Using Environmental Topography.” Nature, vol. 582, Springer Nature, 2020, pp. 582–585, doi:10.1038/s41586-020-2283-z. short: A. Reversat, F.R. Gärtner, J. Merrin, J.A. Stopp, S. Tasciyan, J.L. Aguilera Servin, I. de Vries, R. Hauschild, M. Hons, M. Piel, A. Callan-Jones, R. Voituriez, M.K. Sixt, Nature 582 (2020) 582–585. date_created: 2020-05-24T22:01:01Z date_published: 2020-06-25T00:00:00Z date_updated: 2024-03-27T23:30:23Z day: '25' department: - _id: NanoFab - _id: Bio - _id: MiSi doi: 10.1038/s41586-020-2283-z ec_funded: 1 external_id: isi: - '000532688300008' intvolume: ' 582' isi: 1 language: - iso: eng month: '06' oa_version: None page: 582–585 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 26018E70-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29911 name: Mechanical adaptation of lamellipodial actin - _id: 260AA4E2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '747687' name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells publication: Nature publication_identifier: eissn: - '14764687' issn: - '00280836' publication_status: published publisher: Springer Nature quality_controlled: '1' related_material: link: - description: News on IST Homepage relation: press_release url: https://ist.ac.at/en/news/off-road-mode-enables-mobile-cells-to-move-freely/ record: - id: '14697' relation: dissertation_contains status: public - id: '12401' relation: dissertation_contains status: public scopus_import: '1' status: public title: Cellular locomotion using environmental topography type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 582 year: '2020' ... --- _id: '8190' article_number: e202007029 article_processing_charge: No article_type: letter_note author: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Anna full_name: Huttenlocher, Anna last_name: Huttenlocher citation: ama: 'Sixt MK, Huttenlocher A. Zena Werb (1945-2020): Cell biology in context. The Journal of Cell Biology. 2020;219(8). doi:10.1083/jcb.202007029' apa: 'Sixt, M. K., & Huttenlocher, A. (2020). Zena Werb (1945-2020): Cell biology in context. The Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.202007029' chicago: 'Sixt, Michael K, and Anna Huttenlocher. “Zena Werb (1945-2020): Cell Biology in Context.” The Journal of Cell Biology. Rockefeller University Press, 2020. https://doi.org/10.1083/jcb.202007029.' ieee: 'M. K. Sixt and A. Huttenlocher, “Zena Werb (1945-2020): Cell biology in context,” The Journal of Cell Biology, vol. 219, no. 8. Rockefeller University Press, 2020.' ista: 'Sixt MK, Huttenlocher A. 2020. Zena Werb (1945-2020): Cell biology in context. The Journal of Cell Biology. 219(8), e202007029.' mla: 'Sixt, Michael K., and Anna Huttenlocher. “Zena Werb (1945-2020): Cell Biology in Context.” The Journal of Cell Biology, vol. 219, no. 8, e202007029, Rockefeller University Press, 2020, doi:10.1083/jcb.202007029.' short: M.K. Sixt, A. Huttenlocher, The Journal of Cell Biology 219 (2020). date_created: 2020-08-02T22:00:57Z date_published: 2020-07-22T00:00:00Z date_updated: 2023-10-17T10:04:49Z day: '22' ddc: - '570' department: - _id: MiSi doi: 10.1083/jcb.202007029 external_id: isi: - '000573631000004' file: - access_level: open_access checksum: 30016d778d266b8e17d01094917873b8 content_type: application/pdf creator: dernst date_created: 2020-08-04T13:11:52Z date_updated: 2021-02-02T23:30:03Z embargo: 2021-02-01 file_id: '8200' file_name: 2020_JCB_Sixt.pdf file_size: 830725 relation: main_file file_date_updated: 2021-02-02T23:30:03Z has_accepted_license: '1' intvolume: ' 219' isi: 1 issue: '8' language: - iso: eng month: '07' oa: 1 oa_version: Published Version publication: The Journal of Cell Biology publication_identifier: eissn: - 1540-8140 publication_status: published publisher: Rockefeller University Press scopus_import: '1' status: public title: 'Zena Werb (1945-2020): Cell biology in context' tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 219 year: '2020' ... --- _id: '6824' abstract: - lang: eng text: Platelets are small anucleate cellular fragments that are released by megakaryocytes and safeguard vascular integrity through a process termed ‘haemostasis’. However, platelets have important roles beyond haemostasis as they contribute to the initiation and coordination of intravascular immune responses. They continuously monitor blood vessel integrity and tightly coordinate vascular trafficking and functions of multiple cell types. In this way platelets act as ‘patrolling officers of the vascular highway’ that help to establish effective immune responses to infections and cancer. Here we discuss the distinct biological features of platelets that allow them to shape immune responses to pathogens and tumour cells, highlighting the parallels between these responses. article_processing_charge: No article_type: original author: - first_name: Florian R full_name: Gärtner, Florian R id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 - first_name: Steffen full_name: Massberg, Steffen last_name: Massberg citation: ama: 'Gärtner FR, Massberg S. Patrolling the vascular borders: Platelets in immunity to infection and cancer. Nature Reviews Immunology. 2019;19(12):747–760. doi:10.1038/s41577-019-0202-z' apa: 'Gärtner, F. R., & Massberg, S. (2019). Patrolling the vascular borders: Platelets in immunity to infection and cancer. Nature Reviews Immunology. Springer Nature. https://doi.org/10.1038/s41577-019-0202-z' chicago: 'Gärtner, Florian R, and Steffen Massberg. “Patrolling the Vascular Borders: Platelets in Immunity to Infection and Cancer.” Nature Reviews Immunology. Springer Nature, 2019. https://doi.org/10.1038/s41577-019-0202-z.' ieee: 'F. R. Gärtner and S. Massberg, “Patrolling the vascular borders: Platelets in immunity to infection and cancer,” Nature Reviews Immunology, vol. 19, no. 12. Springer Nature, pp. 747–760, 2019.' ista: 'Gärtner FR, Massberg S. 2019. Patrolling the vascular borders: Platelets in immunity to infection and cancer. Nature Reviews Immunology. 19(12), 747–760.' mla: 'Gärtner, Florian R., and Steffen Massberg. “Patrolling the Vascular Borders: Platelets in Immunity to Infection and Cancer.” Nature Reviews Immunology, vol. 19, no. 12, Springer Nature, 2019, pp. 747–760, doi:10.1038/s41577-019-0202-z.' short: F.R. Gärtner, S. Massberg, Nature Reviews Immunology 19 (2019) 747–760. date_created: 2019-08-20T17:24:32Z date_published: 2019-12-01T00:00:00Z date_updated: 2023-08-29T07:16:14Z day: '01' department: - _id: MiSi doi: 10.1038/s41577-019-0202-z ec_funded: 1 external_id: isi: - '000499090600011' pmid: - '31409920' intvolume: ' 19' isi: 1 issue: '12' language: - iso: eng month: '12' oa_version: None page: 747–760 pmid: 1 project: - _id: 260AA4E2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '747687' name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells publication: Nature Reviews Immunology publication_identifier: eissn: - 1474-1741 issn: - 1474-1733 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: 'Patrolling the vascular borders: Platelets in immunity to infection and cancer' type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 19 year: '2019' ... --- _id: '7009' abstract: - lang: eng text: Cell migration is essential for physiological processes as diverse as development, immune defence and wound healing. It is also a hallmark of cancer malignancy. Thousands of publications have elucidated detailed molecular and biophysical mechanisms of cultured cells migrating on flat, 2D substrates of glass and plastic. However, much less is known about how cells successfully navigate the complex 3D environments of living tissues. In these more complex, native environments, cells use multiple modes of migration, including mesenchymal, amoeboid, lobopodial and collective, and these are governed by the local extracellular microenvironment, specific modalities of Rho GTPase signalling and non- muscle myosin contractility. Migration through 3D environments is challenging because it requires the cell to squeeze through complex or dense extracellular structures. Doing so requires specific cellular adaptations to mechanical features of the extracellular matrix (ECM) or its remodelling. In addition, besides navigating through diverse ECM environments and overcoming extracellular barriers, cells often interact with neighbouring cells and tissues through physical and signalling interactions. Accordingly, cells need to call on an impressively wide diversity of mechanisms to meet these challenges. This Review examines how cells use both classical and novel mechanisms of locomotion as they traverse challenging 3D matrices and cellular environments. It focuses on principles rather than details of migratory mechanisms and draws comparisons between 1D, 2D and 3D migration. article_processing_charge: No article_type: review author: - first_name: KM full_name: Yamada, KM last_name: Yamada - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Yamada K, Sixt MK. Mechanisms of 3D cell migration. Nature Reviews Molecular Cell Biology. 2019;20(12):738–752. doi:10.1038/s41580-019-0172-9 apa: Yamada, K., & Sixt, M. K. (2019). Mechanisms of 3D cell migration. Nature Reviews Molecular Cell Biology. Springer Nature. https://doi.org/10.1038/s41580-019-0172-9 chicago: Yamada, KM, and Michael K Sixt. “Mechanisms of 3D Cell Migration.” Nature Reviews Molecular Cell Biology. Springer Nature, 2019. https://doi.org/10.1038/s41580-019-0172-9. ieee: K. Yamada and M. K. Sixt, “Mechanisms of 3D cell migration,” Nature Reviews Molecular Cell Biology, vol. 20, no. 12. Springer Nature, pp. 738–752, 2019. ista: Yamada K, Sixt MK. 2019. Mechanisms of 3D cell migration. Nature Reviews Molecular Cell Biology. 20(12), 738–752. mla: Yamada, KM, and Michael K. Sixt. “Mechanisms of 3D Cell Migration.” Nature Reviews Molecular Cell Biology, vol. 20, no. 12, Springer Nature, 2019, pp. 738–752, doi:10.1038/s41580-019-0172-9. short: K. Yamada, M.K. Sixt, Nature Reviews Molecular Cell Biology 20 (2019) 738–752. date_created: 2019-11-12T14:54:42Z date_published: 2019-12-01T00:00:00Z date_updated: 2023-08-30T07:22:20Z day: '01' department: - _id: MiSi doi: 10.1038/s41580-019-0172-9 external_id: isi: - '000497966900007' pmid: - '31582855' intvolume: ' 20' isi: 1 issue: '12' language: - iso: eng month: '12' oa_version: None page: 738–752 pmid: 1 publication: Nature Reviews Molecular Cell Biology publication_identifier: eissn: - 1471-0080 issn: - 1471-0072 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Mechanisms of 3D cell migration type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 20 year: '2019' ... --- _id: '6988' abstract: - lang: eng text: 'Platelets are central players in thrombosis and hemostasis but are increasingly recognized as key components of the immune system. They shape ensuing immune responses by recruiting leukocytes, and support the development of adaptive immunity. Recent data shed new light on the complex role of platelets in immunity. Here, we summarize experimental and clinical data on the role of platelets in host defense against bacteria. Platelets bind, contain, and kill bacteria directly; however, platelet proinflammatory effector functions and cross-talk with the coagulation system, can also result in damage to the host (e.g., acute lung injury and sepsis). Novel clinical insights support this dichotomy: platelet inhibition/thrombocytopenia can be either harmful or protective, depending on pathophysiological context. Clinical studies are currently addressing this aspect in greater depth.' article_processing_charge: No article_type: review author: - first_name: Leo full_name: Nicolai, Leo last_name: Nicolai - first_name: Florian R full_name: Gärtner, Florian R id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 - first_name: Steffen full_name: Massberg, Steffen last_name: Massberg citation: ama: 'Nicolai L, Gärtner FR, Massberg S. Platelets in host defense: Experimental and clinical insights. Trends in Immunology. 2019;40(10):922-938. doi:10.1016/j.it.2019.08.004' apa: 'Nicolai, L., Gärtner, F. R., & Massberg, S. (2019). Platelets in host defense: Experimental and clinical insights. Trends in Immunology. Cell Press. https://doi.org/10.1016/j.it.2019.08.004' chicago: 'Nicolai, Leo, Florian R Gärtner, and Steffen Massberg. “Platelets in Host Defense: Experimental and Clinical Insights.” Trends in Immunology. Cell Press, 2019. https://doi.org/10.1016/j.it.2019.08.004.' ieee: 'L. Nicolai, F. R. Gärtner, and S. Massberg, “Platelets in host defense: Experimental and clinical insights,” Trends in Immunology, vol. 40, no. 10. Cell Press, pp. 922–938, 2019.' ista: 'Nicolai L, Gärtner FR, Massberg S. 2019. Platelets in host defense: Experimental and clinical insights. Trends in Immunology. 40(10), 922–938.' mla: 'Nicolai, Leo, et al. “Platelets in Host Defense: Experimental and Clinical Insights.” Trends in Immunology, vol. 40, no. 10, Cell Press, 2019, pp. 922–38, doi:10.1016/j.it.2019.08.004.' short: L. Nicolai, F.R. Gärtner, S. Massberg, Trends in Immunology 40 (2019) 922–938. date_created: 2019-11-04T16:27:36Z date_published: 2019-10-01T00:00:00Z date_updated: 2023-08-30T07:19:23Z day: '01' department: - _id: MiSi doi: 10.1016/j.it.2019.08.004 ec_funded: 1 external_id: isi: - '000493292100005' pmid: - '31601520' intvolume: ' 40' isi: 1 issue: '10' language: - iso: eng month: '10' oa_version: None page: 922-938 pmid: 1 project: - _id: 260AA4E2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '747687' name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells publication: Trends in Immunology publication_identifier: issn: - 1471-4906 publication_status: published publisher: Cell Press quality_controlled: '1' scopus_import: '1' status: public title: 'Platelets in host defense: Experimental and clinical insights' type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 40 year: '2019' ... --- _id: '6979' article_processing_charge: No article_type: original author: - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Kopf A, Sixt MK. Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal. Current Biology. 2019;29(20):R1091-R1093. doi:10.1016/j.cub.2019.08.068' apa: 'Kopf, A., & Sixt, M. K. (2019). Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2019.08.068' chicago: 'Kopf, Aglaja, and Michael K Sixt. “Gut Homeostasis: Active Migration of Intestinal Epithelial Cells in Tissue Renewal.” Current Biology. Cell Press, 2019. https://doi.org/10.1016/j.cub.2019.08.068.' ieee: 'A. Kopf and M. K. Sixt, “Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal,” Current Biology, vol. 29, no. 20. Cell Press, pp. R1091–R1093, 2019.' ista: 'Kopf A, Sixt MK. 2019. Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal. Current Biology. 29(20), R1091–R1093.' mla: 'Kopf, Aglaja, and Michael K. Sixt. “Gut Homeostasis: Active Migration of Intestinal Epithelial Cells in Tissue Renewal.” Current Biology, vol. 29, no. 20, Cell Press, 2019, pp. R1091–93, doi:10.1016/j.cub.2019.08.068.' short: A. Kopf, M.K. Sixt, Current Biology 29 (2019) R1091–R1093. date_created: 2019-11-04T15:18:29Z date_published: 2019-10-21T00:00:00Z date_updated: 2023-09-05T12:43:43Z day: '21' department: - _id: MiSi doi: 10.1016/j.cub.2019.08.068 external_id: isi: - '000491286200016' pmid: - '31639357' intvolume: ' 29' isi: 1 issue: '20' language: - iso: eng month: '10' oa_version: None page: R1091-R1093 pmid: 1 publication: Current Biology publication_identifier: eissn: - 1879-0445 issn: - 0960-9822 publication_status: published publisher: Cell Press quality_controlled: '1' scopus_import: '1' status: public title: 'Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal' type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 29 year: '2019' ... --- _id: '7105' abstract: - lang: eng text: Cell migration is hypothesized to involve a cycle of behaviours beginning with leading edge extension. However, recent evidence suggests that the leading edge may be dispensable for migration, raising the question of what actually controls cell directionality. Here, we exploit the embryonic migration of Drosophila macrophages to bridge the different temporal scales of the behaviours controlling motility. This approach reveals that edge fluctuations during random motility are not persistent and are weakly correlated with motion. In contrast, flow of the actin network behind the leading edge is highly persistent. Quantification of actin flow structure during migration reveals a stable organization and asymmetry in the cell-wide flowfield that strongly correlates with cell directionality. This organization is regulated by a gradient of actin network compression and destruction, which is controlled by myosin contraction and cofilin-mediated disassembly. It is this stable actin-flow polarity, which integrates rapid fluctuations of the leading edge, that controls inherent cellular persistence. article_processing_charge: No article_type: original author: - first_name: Lawrence full_name: Yolland, Lawrence last_name: Yolland - first_name: Mubarik full_name: Burki, Mubarik last_name: Burki - first_name: Stefania full_name: Marcotti, Stefania last_name: Marcotti - first_name: Andrei full_name: Luchici, Andrei last_name: Luchici - first_name: Fiona N. full_name: Kenny, Fiona N. last_name: Kenny - first_name: John Robert full_name: Davis, John Robert last_name: Davis - first_name: Eduardo full_name: Serna-Morales, Eduardo last_name: Serna-Morales - first_name: Jan full_name: Müller, Jan id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D last_name: Müller - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Andrew full_name: Davidson, Andrew last_name: Davidson - first_name: Will full_name: Wood, Will last_name: Wood - first_name: Linus J. full_name: Schumacher, Linus J. last_name: Schumacher - first_name: Robert G. full_name: Endres, Robert G. last_name: Endres - first_name: Mark full_name: Miodownik, Mark last_name: Miodownik - first_name: Brian M. full_name: Stramer, Brian M. last_name: Stramer citation: ama: Yolland L, Burki M, Marcotti S, et al. Persistent and polarized global actin flow is essential for directionality during cell migration. Nature Cell Biology. 2019;21(11):1370-1381. doi:10.1038/s41556-019-0411-5 apa: Yolland, L., Burki, M., Marcotti, S., Luchici, A., Kenny, F. N., Davis, J. R., … Stramer, B. M. (2019). Persistent and polarized global actin flow is essential for directionality during cell migration. Nature Cell Biology. Springer Nature. https://doi.org/10.1038/s41556-019-0411-5 chicago: Yolland, Lawrence, Mubarik Burki, Stefania Marcotti, Andrei Luchici, Fiona N. Kenny, John Robert Davis, Eduardo Serna-Morales, et al. “Persistent and Polarized Global Actin Flow Is Essential for Directionality during Cell Migration.” Nature Cell Biology. Springer Nature, 2019. https://doi.org/10.1038/s41556-019-0411-5. ieee: L. Yolland et al., “Persistent and polarized global actin flow is essential for directionality during cell migration,” Nature Cell Biology, vol. 21, no. 11. Springer Nature, pp. 1370–1381, 2019. ista: Yolland L, Burki M, Marcotti S, Luchici A, Kenny FN, Davis JR, Serna-Morales E, Müller J, Sixt MK, Davidson A, Wood W, Schumacher LJ, Endres RG, Miodownik M, Stramer BM. 2019. Persistent and polarized global actin flow is essential for directionality during cell migration. Nature Cell Biology. 21(11), 1370–1381. mla: Yolland, Lawrence, et al. “Persistent and Polarized Global Actin Flow Is Essential for Directionality during Cell Migration.” Nature Cell Biology, vol. 21, no. 11, Springer Nature, 2019, pp. 1370–81, doi:10.1038/s41556-019-0411-5. short: L. Yolland, M. Burki, S. Marcotti, A. Luchici, F.N. Kenny, J.R. Davis, E. Serna-Morales, J. Müller, M.K. Sixt, A. Davidson, W. Wood, L.J. Schumacher, R.G. Endres, M. Miodownik, B.M. Stramer, Nature Cell Biology 21 (2019) 1370–1381. date_created: 2019-11-25T08:55:00Z date_published: 2019-11-01T00:00:00Z date_updated: 2023-09-06T11:08:52Z day: '01' department: - _id: MiSi doi: 10.1038/s41556-019-0411-5 external_id: isi: - '000495888300009' pmid: - '31685997' intvolume: ' 21' isi: 1 issue: '11' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7025891 month: '11' oa: 1 oa_version: Submitted Version page: 1370-1381 pmid: 1 publication: Nature Cell Biology publication_identifier: eissn: - 1476-4679 issn: - 1465-7392 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Persistent and polarized global actin flow is essential for directionality during cell migration type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 21 year: '2019' ... --- _id: '7420' abstract: - lang: eng text: β1-integrins mediate cell–matrix interactions and their trafficking is important in the dynamic regulation of cell adhesion, migration and malignant processes, including cancer cell invasion. Here, we employ an RNAi screen to characterize regulators of integrin traffic and identify the association of Golgi-localized gamma ear-containing Arf-binding protein 2 (GGA2) with β1-integrin, and its role in recycling of active but not inactive β1-integrin receptors. Silencing of GGA2 limits active β1-integrin levels in focal adhesions and decreases cancer cell migration and invasion, which is in agreement with its ability to regulate the dynamics of active integrins. By using the proximity-dependent biotin identification (BioID) method, we identified two RAB family small GTPases, i.e. RAB13 and RAB10, as novel interactors of GGA2. Functionally, RAB13 silencing triggers the intracellular accumulation of active β1-integrin, and reduces integrin activity in focal adhesions and cell migration similarly to GGA2 depletion, indicating that both facilitate active β1-integrin recycling to the plasma membrane. Thus, GGA2 and RAB13 are important specificity determinants for integrin activity-dependent traffic. article_number: jcs233387 article_processing_charge: No article_type: original author: - first_name: Pranshu full_name: Sahgal, Pranshu last_name: Sahgal - first_name: Jonna H full_name: Alanko, Jonna H id: 2CC12E8C-F248-11E8-B48F-1D18A9856A87 last_name: Alanko orcid: 0000-0002-7698-3061 - first_name: Jaroslav full_name: Icha, Jaroslav last_name: Icha - first_name: Ilkka full_name: Paatero, Ilkka last_name: Paatero - first_name: Hellyeh full_name: Hamidi, Hellyeh last_name: Hamidi - first_name: Antti full_name: Arjonen, Antti last_name: Arjonen - first_name: Mika full_name: Pietilä, Mika last_name: Pietilä - first_name: Anne full_name: Rokka, Anne last_name: Rokka - first_name: Johanna full_name: Ivaska, Johanna last_name: Ivaska citation: ama: Sahgal P, Alanko JH, Icha J, et al. GGA2 and RAB13 promote activity-dependent β1-integrin recycling. Journal of Cell Science. 2019;132(11). doi:10.1242/jcs.233387 apa: Sahgal, P., Alanko, J. H., Icha, J., Paatero, I., Hamidi, H., Arjonen, A., … Ivaska, J. (2019). GGA2 and RAB13 promote activity-dependent β1-integrin recycling. Journal of Cell Science. The Company of Biologists. https://doi.org/10.1242/jcs.233387 chicago: Sahgal, Pranshu, Jonna H Alanko, Jaroslav Icha, Ilkka Paatero, Hellyeh Hamidi, Antti Arjonen, Mika Pietilä, Anne Rokka, and Johanna Ivaska. “GGA2 and RAB13 Promote Activity-Dependent Β1-Integrin Recycling.” Journal of Cell Science. The Company of Biologists, 2019. https://doi.org/10.1242/jcs.233387. ieee: P. Sahgal et al., “GGA2 and RAB13 promote activity-dependent β1-integrin recycling,” Journal of Cell Science, vol. 132, no. 11. The Company of Biologists, 2019. ista: Sahgal P, Alanko JH, Icha J, Paatero I, Hamidi H, Arjonen A, Pietilä M, Rokka A, Ivaska J. 2019. GGA2 and RAB13 promote activity-dependent β1-integrin recycling. Journal of Cell Science. 132(11), jcs233387. mla: Sahgal, Pranshu, et al. “GGA2 and RAB13 Promote Activity-Dependent Β1-Integrin Recycling.” Journal of Cell Science, vol. 132, no. 11, jcs233387, The Company of Biologists, 2019, doi:10.1242/jcs.233387. short: P. Sahgal, J.H. Alanko, J. Icha, I. Paatero, H. Hamidi, A. Arjonen, M. Pietilä, A. Rokka, J. Ivaska, Journal of Cell Science 132 (2019). date_created: 2020-01-30T10:31:42Z date_published: 2019-06-07T00:00:00Z date_updated: 2023-09-06T15:01:00Z day: '07' department: - _id: MiSi doi: 10.1242/jcs.233387 external_id: isi: - '000473327900017' pmid: - '31076515' intvolume: ' 132' isi: 1 issue: '11' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1242/jcs.233387 month: '06' oa: 1 oa_version: Published Version pmid: 1 publication: Journal of Cell Science publication_identifier: eissn: - 1477-9137 issn: - 0021-9533 publication_status: published publisher: The Company of Biologists quality_controlled: '1' status: public title: GGA2 and RAB13 promote activity-dependent β1-integrin recycling type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 132 year: '2019' ... --- _id: '7404' abstract: - lang: eng text: The formation of neuronal dendrite branches is fundamental for the wiring and function of the nervous system. Indeed, dendrite branching enhances the coverage of the neuron's receptive field and modulates the initial processing of incoming stimuli. Complex dendrite patterns are achieved in vivo through a dynamic process of de novo branch formation, branch extension and retraction. The first step towards branch formation is the generation of a dynamic filopodium-like branchlet. The mechanisms underlying the initiation of dendrite branchlets are therefore crucial to the shaping of dendrites. Through in vivo time-lapse imaging of the subcellular localization of actin during the process of branching of Drosophila larva sensory neurons, combined with genetic analysis and electron tomography, we have identified the Actin-related protein (Arp) 2/3 complex as the major actin nucleator involved in the initiation of dendrite branchlet formation, under the control of the activator WAVE and of the small GTPase Rac1. Transient recruitment of an Arp2/3 component marks the site of branchlet initiation in vivo. These data position the activation of Arp2/3 as an early hub for the initiation of branchlet formation. article_number: dev171397 article_processing_charge: No article_type: original author: - first_name: Tomke full_name: Stürner, Tomke last_name: Stürner - first_name: Anastasia full_name: Tatarnikova, Anastasia last_name: Tatarnikova - first_name: Jan full_name: Müller, Jan id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D last_name: Müller - first_name: Barbara full_name: Schaffran, Barbara last_name: Schaffran - first_name: Hermann full_name: Cuntz, Hermann last_name: Cuntz - first_name: Yun full_name: Zhang, Yun last_name: Zhang - first_name: Maria full_name: Nemethova, Maria id: 34E27F1C-F248-11E8-B48F-1D18A9856A87 last_name: Nemethova - first_name: Sven full_name: Bogdan, Sven last_name: Bogdan - first_name: Vic full_name: Small, Vic last_name: Small - first_name: Gaia full_name: Tavosanis, Gaia last_name: Tavosanis citation: ama: Stürner T, Tatarnikova A, Müller J, et al. Transient localization of the Arp2/3 complex initiates neuronal dendrite branching in vivo. Development. 2019;146(7). doi:10.1242/dev.171397 apa: Stürner, T., Tatarnikova, A., Müller, J., Schaffran, B., Cuntz, H., Zhang, Y., … Tavosanis, G. (2019). Transient localization of the Arp2/3 complex initiates neuronal dendrite branching in vivo. Development. The Company of Biologists. https://doi.org/10.1242/dev.171397 chicago: Stürner, Tomke, Anastasia Tatarnikova, Jan Müller, Barbara Schaffran, Hermann Cuntz, Yun Zhang, Maria Nemethova, Sven Bogdan, Vic Small, and Gaia Tavosanis. “Transient Localization of the Arp2/3 Complex Initiates Neuronal Dendrite Branching in Vivo.” Development. The Company of Biologists, 2019. https://doi.org/10.1242/dev.171397. ieee: T. Stürner et al., “Transient localization of the Arp2/3 complex initiates neuronal dendrite branching in vivo,” Development, vol. 146, no. 7. The Company of Biologists, 2019. ista: Stürner T, Tatarnikova A, Müller J, Schaffran B, Cuntz H, Zhang Y, Nemethova M, Bogdan S, Small V, Tavosanis G. 2019. Transient localization of the Arp2/3 complex initiates neuronal dendrite branching in vivo. Development. 146(7), dev171397. mla: Stürner, Tomke, et al. “Transient Localization of the Arp2/3 Complex Initiates Neuronal Dendrite Branching in Vivo.” Development, vol. 146, no. 7, dev171397, The Company of Biologists, 2019, doi:10.1242/dev.171397. short: T. Stürner, A. Tatarnikova, J. Müller, B. Schaffran, H. Cuntz, Y. Zhang, M. Nemethova, S. Bogdan, V. Small, G. Tavosanis, Development 146 (2019). date_created: 2020-01-29T16:27:10Z date_published: 2019-04-04T00:00:00Z date_updated: 2023-09-07T14:47:00Z day: '04' department: - _id: MiSi doi: 10.1242/dev.171397 external_id: isi: - '000464583200006' pmid: - '30910826' intvolume: ' 146' isi: 1 issue: '7' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1242/dev.171397 month: '04' oa: 1 oa_version: Published Version pmid: 1 publication: Development publication_identifier: eissn: - 1477-9129 issn: - 0950-1991 publication_status: published publisher: The Company of Biologists quality_controlled: '1' scopus_import: '1' status: public title: Transient localization of the Arp2/3 complex initiates neuronal dendrite branching in vivo type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 146 year: '2019' ... --- _id: '6947' abstract: - lang: eng text: Lymph nodes are es s ential organs of the immune s ys tem where adaptive immune responses originate, and consist of various leukocyte populations and a stromal backbone. Fibroblastic reticular cells (FRCs) are the main stromal cells and form a sponge-like extracellular matrix network, called conduits , which they thems elves enwrap and contract. Lymph, containing s oluble antigens , arrive in lymph nodes via afferent lymphatic vessels that connect to the s ubcaps ular s inus and conduit network. According to the current paradigm, the conduit network dis tributes afferent lymph through lymph nodes and thus provides acces s for immune cells to lymph-borne antigens. An elas tic caps ule s urrounds the organ and confines the immune cells and FRC network. Lymph nodes are completely packed with lymphocytes and lymphocyte numbers directly dictates the size of the organ. Although lymphocytes cons tantly enter and leave the lymph node, its s ize remains remarkedly s table under homeostatic conditions. It is only partly known how the cellularity and s ize of the lymph node is regulated and how the lymph node is able to swell in inflammation. The role of the FRC network in lymph node s welling and trans fer of fluids are inves tigated in this thes is. Furthermore, we s tudied what trafficking routes are us ed by cancer cells in lymph nodes to form distal metastases.We examined the role of a mechanical feedback in regulation of lymph node swelling. Using parallel plate compression and UV-las er cutting experiments we dis s ected the mechanical force dynamics of the whole lymph node, and individually for FRCs and the caps ule. Physical forces generated by packed lymphocytes directly affect the tens ion on the FRC network and capsule, which increases its resistance to swelling. This implies a feedback mechanism between tis s ue pres s ure and ability of lymphocytes to enter the organ. Following inflammation, the lymph node swells ∼10 fold in two weeks . Yet, what is the role for tens ion on the FRC network and caps ule, and how are lymphocytes able to enter in conditions that resist swelling remain open ques tions . We s how that tens ion on the FRC network is important to limit the swelling rate of the organ so that the FRC network can grow in a coordinated fashion. This is illustrated by interfering with FRC contractility, which leads to faster swelling rates and a dis organized FRC network in the inflamed lymph node. Growth of the FRC network in turn is expected to releas e tens ion on thes e s tructures and lowers the res is tance to swelling, thereby allowing more lymphocytes to enter the organ and drive more swelling. Halt of swelling coincides with a thickening of the caps ule, which forms a thick res is tant band around the organ and lowers tens ion on the FRC network to form a new force equilibrium.The FRC and conduit network are further believed to be a privileged s ite of s oluble information within the lymph node, although many details remain uns olved. We s how by 3D ultra-recons truction that FRCs and antigen pres enting cells cover the s urface of conduit s ys tem for more than 99% and we dis cus s the implications for s oluble information exchangeat the conduit level.Finally, there is an ongoing debate in the cancer field whether and how cancer cells in lymph nodes s eed dis tal metas tas es . We s how that cancer cells infus ed into the lymph node can utilize trafficking routes of immune cells and rapidly migrate to blood vessels. Once in the blood circulation, these cells are able to form metastases in distal tissues. acknowledged_ssus: - _id: Bio - _id: PreCl - _id: EM-Fac alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Frank P full_name: Assen, Frank P id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87 last_name: Assen orcid: 0000-0003-3470-6119 citation: ama: 'Assen FP. Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking. 2019. doi:10.15479/AT:ISTA:6947' apa: 'Assen, F. P. (2019). Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:6947' chicago: 'Assen, Frank P. “Lymph Node Mechanics: Deciphering the Interplay between Stroma Contractility, Morphology and Lymphocyte Trafficking.” Institute of Science and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:6947.' ieee: 'F. P. Assen, “Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking,” Institute of Science and Technology Austria, 2019.' ista: 'Assen FP. 2019. Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking. Institute of Science and Technology Austria.' mla: 'Assen, Frank P. Lymph Node Mechanics: Deciphering the Interplay between Stroma Contractility, Morphology and Lymphocyte Trafficking. Institute of Science and Technology Austria, 2019, doi:10.15479/AT:ISTA:6947.' short: 'F.P. Assen, Lymph Node Mechanics: Deciphering the Interplay between Stroma Contractility, Morphology and Lymphocyte Trafficking, Institute of Science and Technology Austria, 2019.' date_created: 2019-10-14T16:54:52Z date_published: 2019-10-09T00:00:00Z date_updated: 2023-09-13T08:50:57Z day: '9' ddc: - '570' degree_awarded: PhD department: - _id: MiSi doi: 10.15479/AT:ISTA:6947 file: - access_level: closed checksum: 53a739752a500f84d0f8ec953cbbd0b6 content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document creator: fassen date_created: 2019-11-06T12:30:02Z date_updated: 2020-11-07T23:30:03Z embargo_to: open_access file_id: '6990' file_name: PhDthesis_FrankAssen_revised2.docx file_size: 214172667 relation: source_file - access_level: open_access checksum: 8c156b65d9347bb599623a4b09f15d15 content_type: application/pdf creator: fassen date_created: 2019-11-06T12:30:57Z date_updated: 2020-11-07T23:30:03Z embargo: 2020-11-06 file_id: '6991' file_name: PhDthesis_FrankAssen_revised2.pdf file_size: 83637532 relation: main_file file_date_updated: 2020-11-07T23:30:03Z has_accepted_license: '1' language: - iso: eng month: '10' oa: 1 oa_version: Published Version page: '142' publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria related_material: record: - id: '664' relation: part_of_dissertation status: public - id: '402' relation: part_of_dissertation status: public status: public supervisor: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 title: 'Lymph node mechanics: Deciphering the interplay between stroma contractility, morphology and lymphocyte trafficking' type: dissertation user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 year: '2019' ... --- _id: '6891' abstract: - lang: eng text: "While cells of mesenchymal or epithelial origin perform their effector functions in a purely anchorage dependent manner, cells derived from the hematopoietic lineage are not committed to operate only within a specific niche. Instead, these cells are able to function autonomously of the molecular composition in a broad range of tissue compartments. By this means, cells of the hematopoietic lineage retain the capacity to disseminate into connective tissue and recirculate between organs, building the foundation for essential processes such as tissue regeneration or immune surveillance. \r\nCells of the immune system, specifically leukocytes, are extraordinarily good at performing this task. These cells are able to flexibly shift their mode of migration between an adhesion-mediated and an adhesion-independent manner, instantaneously accommodating for any changes in molecular composition of the external scaffold. The key component driving directed leukocyte migration is the chemokine receptor 7, which guides the cell along gradients of chemokine ligand. Therefore, the physical destination of migrating leukocytes is purely deterministic, i.e. given by global directional cues such as chemokine gradients. \r\nNevertheless, these cells typically reside in three-dimensional scaffolds of inhomogeneous complexity, raising the question whether cells are able to locally discriminate between multiple optional migration routes. Current literature provides evidence that leukocytes, specifically dendritic cells, do indeed probe their surrounding by virtue of multiple explorative protrusions. However, it remains enigmatic how these cells decide which one is the more favorable route to follow and what are the key players involved in performing this task. Due to the heterogeneous environment of most tissues, and the vast adaptability of migrating leukocytes, at this time it is not clear to what extent leukocytes are able to optimize their migratory strategy by adapting their level of adhesiveness. And, given the fact that leukocyte migration is characterized by branched cell shapes in combination with high migration velocities, it is reasonable to assume that these cells require fine tuned shape maintenance mechanisms that tightly coordinate protrusion and adhesion dynamics in a spatiotemporal manner. \r\nTherefore, this study aimed to elucidate how rapidly migrating leukocytes opt for an ideal migratory path while maintaining a continuous cell shape and balancing adhesive forces to efficiently navigate through complex microenvironments. \r\nThe results of this study unraveled a role for the microtubule cytoskeleton in promoting the decision making process during path finding and for the first time point towards a microtubule-mediated function in cell shape maintenance of highly ramified cells such as dendritic cells. Furthermore, we found that migrating low-adhesive leukocytes are able to instantaneously adapt to increased tensile load by engaging adhesion receptors. This response was only occurring tangential to the substrate while adhesive properties in the vertical direction were not increased. As leukocytes are primed for rapid migration velocities, these results demonstrate that leukocyte integrins are able to confer a high level of traction forces parallel to the cell membrane along the direction of migration without wasting energy in gluing the cell to the substrate. \r\nThus, the data in the here presented thesis provide new insights into the pivotal role of cytoskeletal dynamics and the mechanisms of force transduction during leukocyte migration. \r\nThereby the here presented results help to further define fundamental principles underlying leukocyte migration and open up potential therapeutic avenues of clinical relevance.\r\n" alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 citation: ama: Kopf A. The implication of cytoskeletal dynamics on leukocyte migration. 2019. doi:10.15479/AT:ISTA:6891 apa: Kopf, A. (2019). The implication of cytoskeletal dynamics on leukocyte migration. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:6891 chicago: Kopf, Aglaja. “The Implication of Cytoskeletal Dynamics on Leukocyte Migration.” Institute of Science and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:6891. ieee: A. Kopf, “The implication of cytoskeletal dynamics on leukocyte migration,” Institute of Science and Technology Austria, 2019. ista: Kopf A. 2019. The implication of cytoskeletal dynamics on leukocyte migration. Institute of Science and Technology Austria. mla: Kopf, Aglaja. The Implication of Cytoskeletal Dynamics on Leukocyte Migration. Institute of Science and Technology Austria, 2019, doi:10.15479/AT:ISTA:6891. short: A. Kopf, The Implication of Cytoskeletal Dynamics on Leukocyte Migration, Institute of Science and Technology Austria, 2019. date_created: 2019-09-19T08:19:44Z date_published: 2019-07-24T00:00:00Z date_updated: 2023-10-18T08:49:17Z day: '24' ddc: - '570' degree_awarded: PhD department: - _id: MiSi doi: 10.15479/AT:ISTA:6891 file: - access_level: closed checksum: 00d100d6468e31e583051e0a006b640c content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document creator: akopf date_created: 2019-10-15T05:28:42Z date_updated: 2020-10-17T22:30:03Z embargo_to: open_access file_id: '6950' file_name: Kopf_PhD_Thesis.docx file_size: 74735267 relation: source_file - access_level: open_access checksum: 5d1baa899993ae6ca81aebebe1797000 content_type: application/pdf creator: akopf date_created: 2019-10-15T05:28:47Z date_updated: 2020-10-17T22:30:03Z embargo: 2020-10-16 file_id: '6951' file_name: Kopf_PhD_Thesis1.pdf file_size: 52787224 relation: main_file file_date_updated: 2020-10-17T22:30:03Z has_accepted_license: '1' keyword: - cell biology - immunology - leukocyte - migration - microfluidics language: - iso: eng month: '07' oa: 1 oa_version: Published Version page: '171' project: - _id: 265E2996-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: W01250-B20 name: Nano-Analytics of Cellular Systems publication_identifier: eissn: - 2663-337X isbn: - 978-3-99078-002-2 publication_status: published publisher: Institute of Science and Technology Austria related_material: link: - relation: press_release url: https://ist.ac.at/en/news/feeling-like-a-cell/ record: - id: '6328' relation: part_of_dissertation status: public - id: '15' relation: part_of_dissertation status: public - id: '6877' relation: part_of_dissertation status: public status: public supervisor: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 title: The implication of cytoskeletal dynamics on leukocyte migration type: dissertation user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 year: '2019' ... --- _id: '6328' abstract: - lang: eng text: During metazoan development, immune surveillance and cancer dissemination, cells migrate in complex three-dimensional microenvironments1,2,3. These spaces are crowded by cells and extracellular matrix, generating mazes with differently sized gaps that are typically smaller than the diameter of the migrating cell4,5. Most mesenchymal and epithelial cells and some—but not all—cancer cells actively generate their migratory path using pericellular tissue proteolysis6. By contrast, amoeboid cells such as leukocytes use non-destructive strategies of locomotion7, raising the question how these extremely fast cells navigate through dense tissues. Here we reveal that leukocytes sample their immediate vicinity for large pore sizes, and are thereby able to choose the path of least resistance. This allows them to circumnavigate local obstacles while effectively following global directional cues such as chemotactic gradients. Pore-size discrimination is facilitated by frontward positioning of the nucleus, which enables the cells to use their bulkiest compartment as a mechanical gauge. Once the nucleus and the closely associated microtubule organizing centre pass the largest pore, cytoplasmic protrusions still lingering in smaller pores are retracted. These retractions are coordinated by dynamic microtubules; when microtubules are disrupted, migrating cells lose coherence and frequently fragment into migratory cytoplasmic pieces. As nuclear positioning in front of the microtubule organizing centre is a typical feature of amoeboid migration, our findings link the fundamental organization of cellular polarity to the strategy of locomotion. acknowledged_ssus: - _id: SSU article_processing_charge: No article_type: letter_note author: - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Julian A full_name: Stopp, Julian A id: 489E3F00-F248-11E8-B48F-1D18A9856A87 last_name: Stopp - first_name: Ingrid full_name: de Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: de Vries - first_name: Meghan K. full_name: Driscoll, Meghan K. last_name: Driscoll - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Erik S. full_name: Welf, Erik S. last_name: Welf - first_name: Gaudenz full_name: Danuser, Gaudenz last_name: Danuser - first_name: Reto full_name: Fiolka, Reto last_name: Fiolka - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Renkawitz J, Kopf A, Stopp JA, et al. Nuclear positioning facilitates amoeboid migration along the path of least resistance. Nature. 2019;568:546-550. doi:10.1038/s41586-019-1087-5 apa: Renkawitz, J., Kopf, A., Stopp, J. A., de Vries, I., Driscoll, M. K., Merrin, J., … Sixt, M. K. (2019). Nuclear positioning facilitates amoeboid migration along the path of least resistance. Nature. Springer Nature. https://doi.org/10.1038/s41586-019-1087-5 chicago: Renkawitz, Jörg, Aglaja Kopf, Julian A Stopp, Ingrid de Vries, Meghan K. Driscoll, Jack Merrin, Robert Hauschild, et al. “Nuclear Positioning Facilitates Amoeboid Migration along the Path of Least Resistance.” Nature. Springer Nature, 2019. https://doi.org/10.1038/s41586-019-1087-5. ieee: J. Renkawitz et al., “Nuclear positioning facilitates amoeboid migration along the path of least resistance,” Nature, vol. 568. Springer Nature, pp. 546–550, 2019. ista: Renkawitz J, Kopf A, Stopp JA, de Vries I, Driscoll MK, Merrin J, Hauschild R, Welf ES, Danuser G, Fiolka R, Sixt MK. 2019. Nuclear positioning facilitates amoeboid migration along the path of least resistance. Nature. 568, 546–550. mla: Renkawitz, Jörg, et al. “Nuclear Positioning Facilitates Amoeboid Migration along the Path of Least Resistance.” Nature, vol. 568, Springer Nature, 2019, pp. 546–50, doi:10.1038/s41586-019-1087-5. short: J. Renkawitz, A. Kopf, J.A. Stopp, I. de Vries, M.K. Driscoll, J. Merrin, R. Hauschild, E.S. Welf, G. Danuser, R. Fiolka, M.K. Sixt, Nature 568 (2019) 546–550. date_created: 2019-04-17T06:52:28Z date_published: 2019-04-25T00:00:00Z date_updated: 2024-03-27T23:30:39Z day: '25' department: - _id: MiSi - _id: NanoFab - _id: Bio doi: 10.1038/s41586-019-1087-5 ec_funded: 1 external_id: isi: - '000465594200050' pmid: - '30944468' intvolume: ' 568' isi: 1 language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217284/ month: '04' oa: 1 oa_version: Submitted Version page: 546-550 pmid: 1 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 265FAEBA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: W01250-B20 name: Nano-Analytics of Cellular Systems - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme - _id: 25A48D24-B435-11E9-9278-68D0E5697425 grant_number: ALTF 1396-2014 name: Molecular and system level view of immune cell migration publication: Nature publication_status: published publisher: Springer Nature quality_controlled: '1' related_material: link: - description: News on IST Homepage relation: press_release url: https://ist.ac.at/en/news/leukocytes-use-their-nucleus-as-a-ruler-to-choose-path-of-least-resistance/ record: - id: '14697' relation: dissertation_contains status: public - id: '6891' relation: dissertation_contains status: public scopus_import: '1' status: public title: Nuclear positioning facilitates amoeboid migration along the path of least resistance type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 568 year: '2019' ... --- _id: '6877' article_processing_charge: No article_type: original author: - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Kopf A, Sixt MK. The neural crest pitches in to remove apoptotic debris. Cell. 2019;179(1):51-53. doi:10.1016/j.cell.2019.08.047 apa: Kopf, A., & Sixt, M. K. (2019). The neural crest pitches in to remove apoptotic debris. Cell. Elsevier. https://doi.org/10.1016/j.cell.2019.08.047 chicago: Kopf, Aglaja, and Michael K Sixt. “The Neural Crest Pitches in to Remove Apoptotic Debris.” Cell. Elsevier, 2019. https://doi.org/10.1016/j.cell.2019.08.047. ieee: A. Kopf and M. K. Sixt, “The neural crest pitches in to remove apoptotic debris,” Cell, vol. 179, no. 1. Elsevier, pp. 51–53, 2019. ista: Kopf A, Sixt MK. 2019. The neural crest pitches in to remove apoptotic debris. Cell. 179(1), 51–53. mla: Kopf, Aglaja, and Michael K. Sixt. “The Neural Crest Pitches in to Remove Apoptotic Debris.” Cell, vol. 179, no. 1, Elsevier, 2019, pp. 51–53, doi:10.1016/j.cell.2019.08.047. short: A. Kopf, M.K. Sixt, Cell 179 (2019) 51–53. date_created: 2019-09-15T22:00:46Z date_published: 2019-09-19T00:00:00Z date_updated: 2024-03-27T23:30:40Z day: '19' department: - _id: MiSi doi: 10.1016/j.cell.2019.08.047 external_id: isi: - '000486618500011' pmid: - '31539498' intvolume: ' 179' isi: 1 issue: '1' language: - iso: eng month: '09' oa_version: None page: 51-53 pmid: 1 publication: Cell publication_identifier: eissn: - 1097-4172 issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' related_material: record: - id: '6891' relation: dissertation_contains status: public scopus_import: '1' status: public title: The neural crest pitches in to remove apoptotic debris type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 179 year: '2019' ... --- _id: '6354' abstract: - lang: eng text: Blood platelets are critical for hemostasis and thrombosis, but also play diverse roles during immune responses. We have recently reported that platelets migrate at sites of infection in vitro and in vivo. Importantly, platelets use their ability to migrate to collect and bundle fibrin (ogen)-bound bacteria accomplishing efficient intravascular bacterial trapping. Here, we describe a method that allows analyzing platelet migration in vitro, focusing on their ability to collect bacteria and trap bacteria under flow. acknowledgement: ' FöFoLe project 947 (F.G.), the Friedrich-Baur-Stiftung project 41/16 (F.G.)' article_number: e3018 author: - first_name: Shuxia full_name: Fan, Shuxia last_name: Fan - first_name: Michael full_name: Lorenz, Michael last_name: Lorenz - first_name: Steffen full_name: Massberg, Steffen last_name: Massberg - first_name: Florian R full_name: Gärtner, Florian R id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 citation: ama: Fan S, Lorenz M, Massberg S, Gärtner FR. Platelet migration and bacterial trapping assay under flow. Bio-Protocol. 2018;8(18). doi:10.21769/bioprotoc.3018 apa: Fan, S., Lorenz, M., Massberg, S., & Gärtner, F. R. (2018). Platelet migration and bacterial trapping assay under flow. Bio-Protocol. Bio-Protocol. https://doi.org/10.21769/bioprotoc.3018 chicago: Fan, Shuxia, Michael Lorenz, Steffen Massberg, and Florian R Gärtner. “Platelet Migration and Bacterial Trapping Assay under Flow.” Bio-Protocol. Bio-Protocol, 2018. https://doi.org/10.21769/bioprotoc.3018. ieee: S. Fan, M. Lorenz, S. Massberg, and F. R. Gärtner, “Platelet migration and bacterial trapping assay under flow,” Bio-Protocol, vol. 8, no. 18. Bio-Protocol, 2018. ista: Fan S, Lorenz M, Massberg S, Gärtner FR. 2018. Platelet migration and bacterial trapping assay under flow. Bio-Protocol. 8(18), e3018. mla: Fan, Shuxia, et al. “Platelet Migration and Bacterial Trapping Assay under Flow.” Bio-Protocol, vol. 8, no. 18, e3018, Bio-Protocol, 2018, doi:10.21769/bioprotoc.3018. short: S. Fan, M. Lorenz, S. Massberg, F.R. Gärtner, Bio-Protocol 8 (2018). date_created: 2019-04-29T09:40:33Z date_published: 2018-09-20T00:00:00Z date_updated: 2021-01-12T08:07:12Z day: '20' ddc: - '570' department: - _id: MiSi doi: 10.21769/bioprotoc.3018 ec_funded: 1 file: - access_level: open_access checksum: d4588377e789da7f360b553ae02c5119 content_type: application/pdf creator: dernst date_created: 2019-04-30T08:04:33Z date_updated: 2020-07-14T12:47:28Z file_id: '6360' file_name: 2018_BioProtocol_Fan.pdf file_size: 2928337 relation: main_file file_date_updated: 2020-07-14T12:47:28Z has_accepted_license: '1' intvolume: ' 8' issue: '18' keyword: - Platelets - Cell migration - Bacteria - Shear flow - Fibrinogen - E. coli language: - iso: eng month: '09' oa: 1 oa_version: Published Version project: - _id: 260AA4E2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '747687' name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells publication: Bio-Protocol publication_identifier: issn: - 2331-8325 publication_status: published publisher: Bio-Protocol quality_controlled: '1' status: public title: Platelet migration and bacterial trapping assay under flow tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2018' ... --- _id: '318' abstract: - lang: eng text: The insect’s fat body combines metabolic and immunological functions. In this issue of Developmental Cell, Franz et al. (2018) show that in Drosophila, cells of the fat body are not static, but can actively “swim” toward sites of epithelial injury, where they physically clog the wound and locally secrete antimicrobial peptides. acknowledgement: Short Survey article_processing_charge: No author: - first_name: Alessandra M full_name: Casano, Alessandra M id: 3DBA3F4E-F248-11E8-B48F-1D18A9856A87 last_name: Casano orcid: 0000-0002-6009-6804 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Casano AM, Sixt MK. A fat lot of good for wound healing. Developmental Cell. 2018;44(4):405-406. doi:10.1016/j.devcel.2018.02.009 apa: Casano, A. M., & Sixt, M. K. (2018). A fat lot of good for wound healing. Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2018.02.009 chicago: Casano, Alessandra M, and Michael K Sixt. “A Fat Lot of Good for Wound Healing.” Developmental Cell. Cell Press, 2018. https://doi.org/10.1016/j.devcel.2018.02.009. ieee: A. M. Casano and M. K. Sixt, “A fat lot of good for wound healing,” Developmental Cell, vol. 44, no. 4. Cell Press, pp. 405–406, 2018. ista: Casano AM, Sixt MK. 2018. A fat lot of good for wound healing. Developmental Cell. 44(4), 405–406. mla: Casano, Alessandra M., and Michael K. Sixt. “A Fat Lot of Good for Wound Healing.” Developmental Cell, vol. 44, no. 4, Cell Press, 2018, pp. 405–06, doi:10.1016/j.devcel.2018.02.009. short: A.M. Casano, M.K. Sixt, Developmental Cell 44 (2018) 405–406. date_created: 2018-12-11T11:45:47Z date_published: 2018-02-26T00:00:00Z date_updated: 2023-09-08T11:42:28Z day: '26' department: - _id: MiSi doi: 10.1016/j.devcel.2018.02.009 external_id: isi: - '000426150700002' pmid: - '29486189' intvolume: ' 44' isi: 1 issue: '4' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pubmed/29486189 month: '02' oa: 1 oa_version: Published Version page: 405 - 406 pmid: 1 publication: Developmental Cell publication_status: published publisher: Cell Press publist_id: '7547' quality_controlled: '1' scopus_import: '1' status: public title: A fat lot of good for wound healing type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 44 year: '2018' ... --- _id: '308' abstract: - lang: eng text: Migrating cells penetrate tissue barriers during development, inflammatory responses, and tumor metastasis. We study if migration in vivo in such three-dimensionally confined environments requires changes in the mechanical properties of the surrounding cells using embryonic Drosophila melanogaster hemocytes, also called macrophages, as a model. We find that macrophage invasion into the germband through transient separation of the apposing ectoderm and mesoderm requires cell deformations and reductions in apical tension in the ectoderm. Interestingly, the genetic pathway governing these mechanical shifts acts downstream of the only known tumor necrosis factor superfamily member in Drosophila, Eiger, and its receptor, Grindelwald. Eiger-Grindelwald signaling reduces levels of active Myosin in the germband ectodermal cortex through the localization of a Crumbs complex component, Patj (Pals-1-associated tight junction protein). We therefore elucidate a distinct molecular pathway that controls tissue tension and demonstrate the importance of such regulation for invasive migration in vivo. acknowledged_ssus: - _id: SSU article_processing_charge: No article_type: original author: - first_name: Aparna full_name: Ratheesh, Aparna id: 2F064CFE-F248-11E8-B48F-1D18A9856A87 last_name: Ratheesh orcid: 0000-0001-7190-0776 - first_name: Julia full_name: Biebl, Julia id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87 last_name: Biebl - first_name: Michael full_name: Smutny, Michael last_name: Smutny - first_name: Jana full_name: Veselá, Jana id: 433253EE-F248-11E8-B48F-1D18A9856A87 last_name: Veselá - first_name: Ekaterina full_name: Papusheva, Ekaterina id: 41DB591E-F248-11E8-B48F-1D18A9856A87 last_name: Papusheva - first_name: Gabriel full_name: Krens, Gabriel id: 2B819732-F248-11E8-B48F-1D18A9856A87 last_name: Krens orcid: 0000-0003-4761-5996 - first_name: Walter full_name: Kaufmann, Walter id: 3F99E422-F248-11E8-B48F-1D18A9856A87 last_name: Kaufmann orcid: 0000-0001-9735-5315 - first_name: Attila full_name: György, Attila id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87 last_name: György orcid: 0000-0002-1819-198X - first_name: Alessandra M full_name: Casano, Alessandra M id: 3DBA3F4E-F248-11E8-B48F-1D18A9856A87 last_name: Casano orcid: 0000-0002-6009-6804 - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 citation: ama: Ratheesh A, Bicher J, Smutny M, et al. Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration. Developmental Cell. 2018;45(3):331-346. doi:10.1016/j.devcel.2018.04.002 apa: Ratheesh, A., Bicher, J., Smutny, M., Veselá, J., Papusheva, E., Krens, G., … Siekhaus, D. E. (2018). Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration. Developmental Cell. Elsevier. https://doi.org/10.1016/j.devcel.2018.04.002 chicago: Ratheesh, Aparna, Julia Bicher, Michael Smutny, Jana Veselá, Ekaterina Papusheva, Gabriel Krens, Walter Kaufmann, Attila György, Alessandra M Casano, and Daria E Siekhaus. “Drosophila TNF Modulates Tissue Tension in the Embryo to Facilitate Macrophage Invasive Migration.” Developmental Cell. Elsevier, 2018. https://doi.org/10.1016/j.devcel.2018.04.002. ieee: A. Ratheesh et al., “Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration,” Developmental Cell, vol. 45, no. 3. Elsevier, pp. 331–346, 2018. ista: Ratheesh A, Bicher J, Smutny M, Veselá J, Papusheva E, Krens G, Kaufmann W, György A, Casano AM, Siekhaus DE. 2018. Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration. Developmental Cell. 45(3), 331–346. mla: Ratheesh, Aparna, et al. “Drosophila TNF Modulates Tissue Tension in the Embryo to Facilitate Macrophage Invasive Migration.” Developmental Cell, vol. 45, no. 3, Elsevier, 2018, pp. 331–46, doi:10.1016/j.devcel.2018.04.002. short: A. Ratheesh, J. Bicher, M. Smutny, J. Veselá, E. Papusheva, G. Krens, W. Kaufmann, A. György, A.M. Casano, D.E. Siekhaus, Developmental Cell 45 (2018) 331–346. date_created: 2018-12-11T11:45:44Z date_published: 2018-05-07T00:00:00Z date_updated: 2023-09-11T13:22:13Z day: '07' department: - _id: DaSi - _id: CaHe - _id: Bio - _id: EM-Fac - _id: MiSi doi: 10.1016/j.devcel.2018.04.002 ec_funded: 1 external_id: isi: - '000432461400009' pmid: - '29738712' intvolume: ' 45' isi: 1 issue: '3' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.devcel.2018.04.002 month: '05' oa: 1 oa_version: Published Version page: 331 - 346 pmid: 1 project: - _id: 253B6E48-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29638 name: Drosophila TNFa´s Funktion in Immunzellen - _id: 2536F660-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '334077' name: Investigating the role of transporters in invasive migration through junctions publication: Developmental Cell publication_status: published publisher: Elsevier quality_controlled: '1' related_material: link: - description: News on IST Homepage relation: press_release url: https://ist.ac.at/en/news/cells-change-tension-to-make-tissue-barriers-easier-to-get-through/ scopus_import: '1' status: public title: Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 45 year: '2018' ... --- _id: '437' abstract: - lang: eng text: Dendritic cells (DCs) are sentinels of the adaptive immune system that reside in peripheral organs of mammals. Upon pathogen encounter, they undergo maturation and up-regulate the chemokine receptor CCR7 that guides them along gradients of its chemokine ligands CCL19 and 21 to the next draining lymph node. There, DCs present peripherally acquired antigen to naïve T cells, thereby triggering adaptive immunity. acknowledged_ssus: - _id: SSU acknowledgement: "This work was supported by grants of the European Research Council (ERC CoG 724373) and the Austrian Science Fund (FWF) to M.S. We thank the scientific support units at IST Austria for excellent technical support.\r\nWe thank the scientific \ support units at IST Austria for excellent technical support. " article_processing_charge: Yes (via OA deal) author: - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Hans full_name: Haecker, Hans last_name: Haecker - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Leithner AF, Renkawitz J, de Vries I, Hauschild R, Haecker H, Sixt MK. Fast and efficient genetic engineering of hematopoietic precursor cells for the study of dendritic cell migration. European Journal of Immunology. 2018;48(6):1074-1077. doi:10.1002/eji.201747358 apa: Leithner, A. F., Renkawitz, J., de Vries, I., Hauschild, R., Haecker, H., & Sixt, M. K. (2018). Fast and efficient genetic engineering of hematopoietic precursor cells for the study of dendritic cell migration. European Journal of Immunology. Wiley-Blackwell. https://doi.org/10.1002/eji.201747358 chicago: Leithner, Alexander F, Jörg Renkawitz, Ingrid de Vries, Robert Hauschild, Hans Haecker, and Michael K Sixt. “Fast and Efficient Genetic Engineering of Hematopoietic Precursor Cells for the Study of Dendritic Cell Migration.” European Journal of Immunology. Wiley-Blackwell, 2018. https://doi.org/10.1002/eji.201747358. ieee: A. F. Leithner, J. Renkawitz, I. de Vries, R. Hauschild, H. Haecker, and M. K. Sixt, “Fast and efficient genetic engineering of hematopoietic precursor cells for the study of dendritic cell migration,” European Journal of Immunology, vol. 48, no. 6. Wiley-Blackwell, pp. 1074–1077, 2018. ista: Leithner AF, Renkawitz J, de Vries I, Hauschild R, Haecker H, Sixt MK. 2018. Fast and efficient genetic engineering of hematopoietic precursor cells for the study of dendritic cell migration. European Journal of Immunology. 48(6), 1074–1077. mla: Leithner, Alexander F., et al. “Fast and Efficient Genetic Engineering of Hematopoietic Precursor Cells for the Study of Dendritic Cell Migration.” European Journal of Immunology, vol. 48, no. 6, Wiley-Blackwell, 2018, pp. 1074–77, doi:10.1002/eji.201747358. short: A.F. Leithner, J. Renkawitz, I. de Vries, R. Hauschild, H. Haecker, M.K. Sixt, European Journal of Immunology 48 (2018) 1074–1077. date_created: 2018-12-11T11:46:28Z date_published: 2018-02-13T00:00:00Z date_updated: 2023-09-11T14:01:18Z day: '13' ddc: - '570' department: - _id: MiSi - _id: Bio doi: 10.1002/eji.201747358 ec_funded: 1 external_id: isi: - '000434963700016' file: - access_level: open_access checksum: 9d5b74cd016505aeb9a4c2d33bbedaeb content_type: application/pdf creator: system date_created: 2018-12-12T10:13:56Z date_updated: 2020-07-14T12:46:27Z file_id: '5044' file_name: IST-2018-1067-v1+2_Leithner_et_al-2018-European_Journal_of_Immunology.pdf file_size: 590106 relation: main_file file_date_updated: 2020-07-14T12:46:27Z has_accepted_license: '1' intvolume: ' 48' isi: 1 issue: '6' language: - iso: eng month: '02' oa: 1 oa_version: Published Version page: 1074 - 1077 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: European Journal of Immunology publication_status: published publisher: Wiley-Blackwell publist_id: '7386' pubrep_id: '1067' quality_controlled: '1' scopus_import: '1' status: public title: Fast and efficient genetic engineering of hematopoietic precursor cells for the study of dendritic cell migration tmp: image: /images/cc_by_nc.png legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) short: CC BY-NC (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 48 year: '2018' ... --- _id: '5672' abstract: - lang: eng text: The release of IgM is the first line of an antibody response and precedes the generation of high affinity IgG in germinal centers. Once secreted by freshly activated plasmablasts, IgM is released into the efferent lymph of reactive lymph nodes as early as 3 d after immunization. As pentameric IgM has an enormous size of 1,000 kD, its diffusibility is low, and one might wonder how it can pass through the densely lymphocyte-packed environment of a lymph node parenchyma in order to reach its exit. In this issue of JEM, Thierry et al. show that, in order to reach the blood stream, IgM molecules take a specific micro-anatomical route via lymph node conduits. article_processing_charge: No author: - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Reversat A, Sixt MK. IgM’s exit route. Journal of Experimental Medicine. 2018;215(12):2959-2961. doi:10.1084/jem.20181934 apa: Reversat, A., & Sixt, M. K. (2018). IgM’s exit route. Journal of Experimental Medicine. Rockefeller University Press. https://doi.org/10.1084/jem.20181934 chicago: Reversat, Anne, and Michael K Sixt. “IgM’s Exit Route.” Journal of Experimental Medicine. Rockefeller University Press, 2018. https://doi.org/10.1084/jem.20181934. ieee: A. Reversat and M. K. Sixt, “IgM’s exit route,” Journal of Experimental Medicine, vol. 215, no. 12. Rockefeller University Press, pp. 2959–2961, 2018. ista: Reversat A, Sixt MK. 2018. IgM’s exit route. Journal of Experimental Medicine. 215(12), 2959–2961. mla: Reversat, Anne, and Michael K. Sixt. “IgM’s Exit Route.” Journal of Experimental Medicine, vol. 215, no. 12, Rockefeller University Press, 2018, pp. 2959–61, doi:10.1084/jem.20181934. short: A. Reversat, M.K. Sixt, Journal of Experimental Medicine 215 (2018) 2959–2961. date_created: 2018-12-16T22:59:18Z date_published: 2018-11-20T00:00:00Z date_updated: 2023-09-11T14:12:06Z day: '20' ddc: - '570' department: - _id: MiSi doi: 10.1084/jem.20181934 external_id: isi: - '000451920600002' file: - access_level: open_access checksum: 687beea1d64c213f4cb9e3c29ec11a14 content_type: application/pdf creator: dernst date_created: 2019-02-06T08:49:52Z date_updated: 2020-07-14T12:47:09Z file_id: '5931' file_name: 2018_JournalExperMed_Reversat.pdf file_size: 1216437 relation: main_file file_date_updated: 2020-07-14T12:47:09Z has_accepted_license: '1' intvolume: ' 215' isi: 1 issue: '12' language: - iso: eng month: '11' oa: 1 oa_version: Published Version page: 2959-2961 publication: Journal of Experimental Medicine publication_identifier: issn: - '00221007' publication_status: published publisher: Rockefeller University Press quality_controlled: '1' scopus_import: '1' status: public title: IgM's exit route tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 215 year: '2018' ... --- _id: '275' abstract: - lang: eng text: Lymphatic endothelial cells (LECs) release extracellular chemokines to guide the migration of dendritic cells. In this study, we report that LECs also release basolateral exosome-rich endothelial vesicles (EEVs) that are secreted in greater numbers in the presence of inflammatory cytokines and accumulate in the perivascular stroma of small lymphatic vessels in human chronic inflammatory diseases. Proteomic analyses of EEV fractions identified > 1,700 cargo proteins and revealed a dominant motility-promoting protein signature. In vitro and ex vivo EEV fractions augmented cellular protrusion formation in a CX3CL1/fractalkine-dependent fashion and enhanced the directional migratory response of human dendritic cells along guidance cues. We conclude that perilymphatic LEC exosomes enhance exploratory behavior and thus promote directional migration of CX3CR1-expressing cells in complex tissue environments. acknowledgement: M. Brown was supported by the Cell Communication in Health and Disease Graduate Study Program of the Austrian Science Fund and Medizinische Universität Wien, M. Sixt by the European Research Council (ERC GA 281556) and an Austrian Science Fund START award, K.L. Bennett by the Austrian Academy of Sciences, D.G. Jackson and L.A. Johnson by Unit Funding (MC_UU_12010/2) and project grants from the Medical Research Council (G1100134 and MR/L008610/1), and M. Detmar by the Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung and Advanced European Research Council grant LYVICAM. K. Vaahtomeri was supported by an Academy of Finland postdoctoral research grant (287853). This project has received funding from the European Union’s Horizon 2020 research and innovation program under grant agreement No. 668036 (RELENT). article_processing_charge: No author: - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Louise full_name: Johnson, Louise last_name: Johnson - first_name: Dario full_name: Leone, Dario last_name: Leone - first_name: Peter full_name: Májek, Peter last_name: Májek - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Daniel full_name: Senfter, Daniel last_name: Senfter - first_name: Nora full_name: Bukosza, Nora last_name: Bukosza - first_name: Helga full_name: Schachner, Helga last_name: Schachner - first_name: Gabriele full_name: Asfour, Gabriele last_name: Asfour - first_name: Brigitte full_name: Langer, Brigitte last_name: Langer - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Katja full_name: Parapatics, Katja last_name: Parapatics - first_name: Young full_name: Hong, Young last_name: Hong - first_name: Keiryn full_name: Bennett, Keiryn last_name: Bennett - first_name: Renate full_name: Kain, Renate last_name: Kain - first_name: Michael full_name: Detmar, Michael last_name: Detmar - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: David full_name: Jackson, David last_name: Jackson - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki citation: ama: Brown M, Johnson L, Leone D, et al. Lymphatic exosomes promote dendritic cell migration along guidance cues. Journal of Cell Biology. 2018;217(6):2205-2221. doi:10.1083/jcb.201612051 apa: Brown, M., Johnson, L., Leone, D., Májek, P., Vaahtomeri, K., Senfter, D., … Kerjaschki, D. (2018). Lymphatic exosomes promote dendritic cell migration along guidance cues. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201612051 chicago: Brown, Markus, Louise Johnson, Dario Leone, Peter Májek, Kari Vaahtomeri, Daniel Senfter, Nora Bukosza, et al. “Lymphatic Exosomes Promote Dendritic Cell Migration along Guidance Cues.” Journal of Cell Biology. Rockefeller University Press, 2018. https://doi.org/10.1083/jcb.201612051. ieee: M. Brown et al., “Lymphatic exosomes promote dendritic cell migration along guidance cues,” Journal of Cell Biology, vol. 217, no. 6. Rockefeller University Press, pp. 2205–2221, 2018. ista: Brown M, Johnson L, Leone D, Májek P, Vaahtomeri K, Senfter D, Bukosza N, Schachner H, Asfour G, Langer B, Hauschild R, Parapatics K, Hong Y, Bennett K, Kain R, Detmar M, Sixt MK, Jackson D, Kerjaschki D. 2018. Lymphatic exosomes promote dendritic cell migration along guidance cues. Journal of Cell Biology. 217(6), 2205–2221. mla: Brown, Markus, et al. “Lymphatic Exosomes Promote Dendritic Cell Migration along Guidance Cues.” Journal of Cell Biology, vol. 217, no. 6, Rockefeller University Press, 2018, pp. 2205–21, doi:10.1083/jcb.201612051. short: M. Brown, L. Johnson, D. Leone, P. Májek, K. Vaahtomeri, D. Senfter, N. Bukosza, H. Schachner, G. Asfour, B. Langer, R. Hauschild, K. Parapatics, Y. Hong, K. Bennett, R. Kain, M. Detmar, M.K. Sixt, D. Jackson, D. Kerjaschki, Journal of Cell Biology 217 (2018) 2205–2221. date_created: 2018-12-11T11:45:33Z date_published: 2018-04-12T00:00:00Z date_updated: 2023-09-13T08:51:29Z day: '12' ddc: - '570' department: - _id: MiSi - _id: Bio doi: 10.1083/jcb.201612051 ec_funded: 1 external_id: isi: - '000438077800026' pmid: - '29650776' file: - access_level: open_access checksum: 9c7eba51a35c62da8c13f98120b64df4 content_type: application/pdf creator: dernst date_created: 2018-12-17T12:50:07Z date_updated: 2020-07-14T12:45:45Z file_id: '5704' file_name: 2018_JournalCellBiology_Brown.pdf file_size: 2252043 relation: main_file file_date_updated: 2020-07-14T12:45:45Z has_accepted_license: '1' intvolume: ' 217' isi: 1 issue: '6' language: - iso: eng month: '04' oa: 1 oa_version: Published Version page: 2205 - 2221 pmid: 1 project: - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Journal of Cell Biology publication_status: published publisher: Rockefeller University Press publist_id: '7627' quality_controlled: '1' scopus_import: '1' status: public title: Lymphatic exosomes promote dendritic cell migration along guidance cues tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 217 year: '2018' ... --- _id: '5858' abstract: - lang: eng text: Spatial patterns are ubiquitous on the subcellular, cellular and tissue level, and can be studied using imaging techniques such as light and fluorescence microscopy. Imaging data provide quantitative information about biological systems; however, mechanisms causing spatial patterning often remain elusive. In recent years, spatio-temporal mathematical modelling has helped to overcome this problem. Yet, outliers and structured noise limit modelling of whole imaging data, and models often consider spatial summary statistics. Here, we introduce an integrated data-driven modelling approach that can cope with measurement artefacts and whole imaging data. Our approach combines mechanistic models of the biological processes with robust statistical models of the measurement process. The parameters of the integrated model are calibrated using a maximum-likelihood approach. We used this integrated modelling approach to study in vivo gradients of the chemokine (C-C motif) ligand 21 (CCL21). CCL21 gradients guide dendritic cells and are important in the adaptive immune response. Using artificial data, we verified that the integrated modelling approach provides reliable parameter estimates in the presence of measurement noise and that bias and variance of these estimates are reduced compared to conventional approaches. The application to experimental data allowed the parametrization and subsequent refinement of the model using additional mechanisms. Among other results, model-based hypothesis testing predicted lymphatic vessel-dependent concentration of heparan sulfate, the binding partner of CCL21. The selected model provided an accurate description of the experimental data and was partially validated using published data. Our findings demonstrate that integrated statistical modelling of whole imaging data is computationally feasible and can provide novel biological insights. article_number: '20180600' article_processing_charge: No author: - first_name: Sabrina full_name: Hross, Sabrina last_name: Hross - first_name: Fabian J. full_name: Theis, Fabian J. last_name: Theis - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Jan full_name: Hasenauer, Jan last_name: Hasenauer citation: ama: Hross S, Theis FJ, Sixt MK, Hasenauer J. Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data. Journal of the Royal Society Interface. 2018;15(149). doi:10.1098/rsif.2018.0600 apa: Hross, S., Theis, F. J., Sixt, M. K., & Hasenauer, J. (2018). Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data. Journal of the Royal Society Interface. Royal Society Publishing. https://doi.org/10.1098/rsif.2018.0600 chicago: Hross, Sabrina, Fabian J. Theis, Michael K Sixt, and Jan Hasenauer. “Mechanistic Description of Spatial Processes Using Integrative Modelling of Noise-Corrupted Imaging Data.” Journal of the Royal Society Interface. Royal Society Publishing, 2018. https://doi.org/10.1098/rsif.2018.0600. ieee: S. Hross, F. J. Theis, M. K. Sixt, and J. Hasenauer, “Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data,” Journal of the Royal Society Interface, vol. 15, no. 149. Royal Society Publishing, 2018. ista: Hross S, Theis FJ, Sixt MK, Hasenauer J. 2018. Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data. Journal of the Royal Society Interface. 15(149), 20180600. mla: Hross, Sabrina, et al. “Mechanistic Description of Spatial Processes Using Integrative Modelling of Noise-Corrupted Imaging Data.” Journal of the Royal Society Interface, vol. 15, no. 149, 20180600, Royal Society Publishing, 2018, doi:10.1098/rsif.2018.0600. short: S. Hross, F.J. Theis, M.K. Sixt, J. Hasenauer, Journal of the Royal Society Interface 15 (2018). date_created: 2019-01-20T22:59:18Z date_published: 2018-12-05T00:00:00Z date_updated: 2023-09-13T08:55:05Z day: '05' ddc: - '570' department: - _id: MiSi doi: 10.1098/rsif.2018.0600 external_id: isi: - '000456783800011' file: - access_level: open_access checksum: 56eb4308a15b7190bff938fab1f780e8 content_type: application/pdf creator: dernst date_created: 2019-02-05T14:46:44Z date_updated: 2020-07-14T12:47:13Z file_id: '5925' file_name: 2018_Interface_Hross.pdf file_size: 1464288 relation: main_file file_date_updated: 2020-07-14T12:47:13Z has_accepted_license: '1' intvolume: ' 15' isi: 1 issue: '149' language: - iso: eng month: '12' oa: 1 oa_version: Published Version publication: Journal of the Royal Society Interface publication_identifier: issn: - '17425689' publication_status: published publisher: Royal Society Publishing quality_controlled: '1' scopus_import: '1' status: public title: Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 15 year: '2018' ... --- _id: '153' abstract: - lang: eng text: Cells migrating in multicellular organisms steadily traverse complex three-dimensional (3D) environments. To decipher the underlying cell biology, current experimental setups either use simplified 2D, tissue-mimetic 3D (e.g., collagen matrices) or in vivo environments. While only in vivo experiments are truly physiological, they do not allow for precise manipulation of environmental parameters. 2D in vitro experiments do allow mechanical and chemical manipulations, but increasing evidence demonstrates substantial differences of migratory mechanisms in 2D and 3D. Here, we describe simple, robust, and versatile “pillar forests” to investigate cell migration in complex but fully controllable 3D environments. Pillar forests are polydimethylsiloxane-based setups, in which two closely adjacent surfaces are interconnected by arrays of micrometer-sized pillars. Changing the pillar shape, size, height and the inter-pillar distance precisely manipulates microenvironmental parameters (e.g., pore sizes, micro-geometry, micro-topology), while being easily combined with chemotactic cues, surface coatings, diverse cell types and advanced imaging techniques. Thus, pillar forests combine the advantages of 2D cell migration assays with the precise definition of 3D environmental parameters. article_processing_charge: No author: - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Renkawitz J, Reversat A, Leithner AF, Merrin J, Sixt MK. Micro-engineered “pillar forests” to study cell migration in complex but controlled 3D environments. In: Methods in Cell Biology. Vol 147. Academic Press; 2018:79-91. doi:10.1016/bs.mcb.2018.07.004' apa: Renkawitz, J., Reversat, A., Leithner, A. F., Merrin, J., & Sixt, M. K. (2018). Micro-engineered “pillar forests” to study cell migration in complex but controlled 3D environments. In Methods in Cell Biology (Vol. 147, pp. 79–91). Academic Press. https://doi.org/10.1016/bs.mcb.2018.07.004 chicago: Renkawitz, Jörg, Anne Reversat, Alexander F Leithner, Jack Merrin, and Michael K Sixt. “Micro-Engineered ‘Pillar Forests’ to Study Cell Migration in Complex but Controlled 3D Environments.” In Methods in Cell Biology, 147:79–91. Academic Press, 2018. https://doi.org/10.1016/bs.mcb.2018.07.004. ieee: J. Renkawitz, A. Reversat, A. F. Leithner, J. Merrin, and M. K. Sixt, “Micro-engineered ‘pillar forests’ to study cell migration in complex but controlled 3D environments,” in Methods in Cell Biology, vol. 147, Academic Press, 2018, pp. 79–91. ista: 'Renkawitz J, Reversat A, Leithner AF, Merrin J, Sixt MK. 2018.Micro-engineered “pillar forests” to study cell migration in complex but controlled 3D environments. In: Methods in Cell Biology. vol. 147, 79–91.' mla: Renkawitz, Jörg, et al. “Micro-Engineered ‘Pillar Forests’ to Study Cell Migration in Complex but Controlled 3D Environments.” Methods in Cell Biology, vol. 147, Academic Press, 2018, pp. 79–91, doi:10.1016/bs.mcb.2018.07.004. short: J. Renkawitz, A. Reversat, A.F. Leithner, J. Merrin, M.K. Sixt, in:, Methods in Cell Biology, Academic Press, 2018, pp. 79–91. date_created: 2018-12-11T11:44:54Z date_published: 2018-07-27T00:00:00Z date_updated: 2023-09-13T08:56:35Z day: '27' department: - _id: MiSi - _id: NanoFab doi: 10.1016/bs.mcb.2018.07.004 external_id: isi: - '000452412300006' pmid: - '30165964' intvolume: ' 147' isi: 1 language: - iso: eng month: '07' oa_version: None page: 79 - 91 pmid: 1 publication: Methods in Cell Biology publication_identifier: issn: - 0091679X publication_status: published publisher: Academic Press publist_id: '7768' quality_controlled: '1' scopus_import: '1' status: public title: Micro-engineered “pillar forests” to study cell migration in complex but controlled 3D environments type: book_chapter user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 147 year: '2018' ... --- _id: '276' abstract: - lang: eng text: Directed migration of cells relies on their ability to sense directional guidance cues and to interact with pericellular structures in order to transduce contractile cytoskeletal- into mechanical forces. These biomechanical processes depend highly on microenvironmental factors such as exposure to 2D surfaces or 3D matrices. In vivo, the majority of cells are exposed to 3D environments. Data on 3D cell migration are mostly derived from intravital microscopy or collagen-based in vitro assays. Both approaches offer only limited controlla-bility of experimental conditions. Here, we developed an automated microfluidic system that allows positioning of cells in 3D microenvironments containing highly controlled diffusion-based chemokine gradients. Tracking migration in such gradients was feasible in real time at the single cell level. Moreover, the setup allowed on-chip immunocytochemistry and thus linking of functional with phenotypical properties in individual cells. Spatially defined retrieval of cells from the device allows down-stream off-chip analysis. Using dendritic cells as a model, our setup specifically allowed us for the first time to quantitate key migration characteristics of cells exposed to identical gradients of the chemokine CCL19 yet placed on 2D vs in 3D environments. Migration properties between 2D and 3D migration were distinct. Morphological features of cells migrating in an in vitro 3D environment were similar to those of cells migrating in animal tissues, but different from cells migrating on a surface. Our system thus offers a highly controllable in vitro-mimic of a 3D environment that cells traffic in vivo. acknowledgement: This work was supported by the Swiss National Science Foundation (MD-PhD fellowships, 323530_164221 to C.F.; and 323630_151483 to A.J.; grant PZ00P3_144863 to M.R, grant 31003A_156431 to T.S.; PZ00P3_148000 to C.T.B.; PZ00P3_154733 to M.M.), a Novartis “FreeNovation” grant to M.M. and T.S. and an EMBO long-term fellowship (ALTF 1396-2014) co-funded by the European Commission (LTFCOFUND2013, GA-2013-609409) to J.R.. M.R. was supported by the Gebert Rüf Foundation (GRS 058/14). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. article_number: e0198330 article_processing_charge: No article_type: original author: - first_name: Corina full_name: Frick, Corina last_name: Frick - first_name: Philip full_name: Dettinger, Philip last_name: Dettinger - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Annaïse full_name: Jauch, Annaïse last_name: Jauch - first_name: Christoph full_name: Berger, Christoph last_name: Berger - first_name: Mike full_name: Recher, Mike last_name: Recher - first_name: Timm full_name: Schroeder, Timm last_name: Schroeder - first_name: Matthias full_name: Mehling, Matthias last_name: Mehling citation: ama: Frick C, Dettinger P, Renkawitz J, et al. Nano-scale microfluidics to study 3D chemotaxis at the single cell level. PLoS One. 2018;13(6). doi:10.1371/journal.pone.0198330 apa: Frick, C., Dettinger, P., Renkawitz, J., Jauch, A., Berger, C., Recher, M., … Mehling, M. (2018). Nano-scale microfluidics to study 3D chemotaxis at the single cell level. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0198330 chicago: Frick, Corina, Philip Dettinger, Jörg Renkawitz, Annaïse Jauch, Christoph Berger, Mike Recher, Timm Schroeder, and Matthias Mehling. “Nano-Scale Microfluidics to Study 3D Chemotaxis at the Single Cell Level.” PLoS One. Public Library of Science, 2018. https://doi.org/10.1371/journal.pone.0198330. ieee: C. Frick et al., “Nano-scale microfluidics to study 3D chemotaxis at the single cell level,” PLoS One, vol. 13, no. 6. Public Library of Science, 2018. ista: Frick C, Dettinger P, Renkawitz J, Jauch A, Berger C, Recher M, Schroeder T, Mehling M. 2018. Nano-scale microfluidics to study 3D chemotaxis at the single cell level. PLoS One. 13(6), e0198330. mla: Frick, Corina, et al. “Nano-Scale Microfluidics to Study 3D Chemotaxis at the Single Cell Level.” PLoS One, vol. 13, no. 6, e0198330, Public Library of Science, 2018, doi:10.1371/journal.pone.0198330. short: C. Frick, P. Dettinger, J. Renkawitz, A. Jauch, C. Berger, M. Recher, T. Schroeder, M. Mehling, PLoS One 13 (2018). date_created: 2018-12-11T11:45:34Z date_published: 2018-06-07T00:00:00Z date_updated: 2023-09-13T09:00:15Z day: '07' ddc: - '570' department: - _id: MiSi doi: 10.1371/journal.pone.0198330 external_id: isi: - '000434384900031' file: - access_level: open_access checksum: 95fc5dc3938b3ad3b7697d10c83cc143 content_type: application/pdf creator: dernst date_created: 2018-12-17T14:10:32Z date_updated: 2020-07-14T12:45:45Z file_id: '5709' file_name: 2018_Plos_Frick.pdf file_size: 7682167 relation: main_file file_date_updated: 2020-07-14T12:45:45Z has_accepted_license: '1' intvolume: ' 13' isi: 1 issue: '6' language: - iso: eng month: '06' oa: 1 oa_version: Published Version publication: PLoS One publication_status: published publisher: Public Library of Science publist_id: '7626' quality_controlled: '1' scopus_import: '1' status: public title: Nano-scale microfluidics to study 3D chemotaxis at the single cell level tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 13 year: '2018' ... --- _id: '5861' abstract: - lang: eng text: In zebrafish larvae, it is the cell type that determines how the cell responds to a chemokine signal. article_number: e37888 article_processing_charge: No article_type: original author: - first_name: Jonna H full_name: Alanko, Jonna H id: 2CC12E8C-F248-11E8-B48F-1D18A9856A87 last_name: Alanko orcid: 0000-0002-7698-3061 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Alanko JH, Sixt MK. The cell sets the tone. eLife. 2018;7. doi:10.7554/eLife.37888 apa: Alanko, J. H., & Sixt, M. K. (2018). The cell sets the tone. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.37888 chicago: Alanko, Jonna H, and Michael K Sixt. “The Cell Sets the Tone.” ELife. eLife Sciences Publications, 2018. https://doi.org/10.7554/eLife.37888. ieee: J. H. Alanko and M. K. Sixt, “The cell sets the tone,” eLife, vol. 7. eLife Sciences Publications, 2018. ista: Alanko JH, Sixt MK. 2018. The cell sets the tone. eLife. 7, e37888. mla: Alanko, Jonna H., and Michael K. Sixt. “The Cell Sets the Tone.” ELife, vol. 7, e37888, eLife Sciences Publications, 2018, doi:10.7554/eLife.37888. short: J.H. Alanko, M.K. Sixt, ELife 7 (2018). date_created: 2019-01-20T22:59:19Z date_published: 2018-06-06T00:00:00Z date_updated: 2023-09-19T10:01:39Z day: '06' ddc: - '570' department: - _id: MiSi doi: 10.7554/eLife.37888 external_id: isi: - '000434375000001' file: - access_level: open_access checksum: f1c7ec2a809408d763c4b529a98f9a3b content_type: application/pdf creator: dernst date_created: 2019-02-13T10:52:11Z date_updated: 2020-07-14T12:47:13Z file_id: '5973' file_name: 2018_eLife_Alanko.pdf file_size: 358141 relation: main_file file_date_updated: 2020-07-14T12:47:13Z has_accepted_license: '1' intvolume: ' 7' isi: 1 language: - iso: eng month: '06' oa: 1 oa_version: Published Version publication: eLife publication_identifier: issn: - 2050084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: The cell sets the tone tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 7 year: '2018' ... --- _id: '5984' abstract: - lang: eng text: G-protein-coupled receptors (GPCRs) form the largest receptor family, relay environmental stimuli to changes in cell behavior and represent prime drug targets. Many GPCRs are classified as orphan receptors because of the limited knowledge on their ligands and coupling to cellular signaling machineries. Here, we engineer a library of 63 chimeric receptors that contain the signaling domains of human orphan and understudied GPCRs functionally linked to the light-sensing domain of rhodopsin. Upon stimulation with visible light, we identify activation of canonical cell signaling pathways, including cAMP-, Ca2+-, MAPK/ERK-, and Rho-dependent pathways, downstream of the engineered receptors. For the human pseudogene GPR33, we resurrect a signaling function that supports its hypothesized role as a pathogen entry site. These results demonstrate that substituting unknown chemical activators with a light switch can reveal information about protein function and provide an optically controlled protein library for exploring the physiology and therapeutic potential of understudied GPCRs. article_number: '1950' article_processing_charge: No author: - first_name: Maurizio full_name: Morri, Maurizio id: 4863116E-F248-11E8-B48F-1D18A9856A87 last_name: Morri - first_name: Inmaculada full_name: Sanchez-Romero, Inmaculada id: 3D9C5D30-F248-11E8-B48F-1D18A9856A87 last_name: Sanchez-Romero - first_name: Alexandra-Madelaine full_name: Tichy, Alexandra-Madelaine id: 29D8BB2C-F248-11E8-B48F-1D18A9856A87 last_name: Tichy - first_name: Stephanie full_name: Kainrath, Stephanie id: 32CFBA64-F248-11E8-B48F-1D18A9856A87 last_name: Kainrath - first_name: Elliot J. full_name: Gerrard, Elliot J. last_name: Gerrard - first_name: Priscila full_name: Hirschfeld, Priscila id: 435ACB3A-F248-11E8-B48F-1D18A9856A87 last_name: Hirschfeld - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Harald L full_name: Janovjak, Harald L id: 33BA6C30-F248-11E8-B48F-1D18A9856A87 last_name: Janovjak orcid: 0000-0002-8023-9315 citation: ama: Morri M, Sanchez-Romero I, Tichy A-M, et al. Optical functionalization of human class A orphan G-protein-coupled receptors. Nature Communications. 2018;9(1). doi:10.1038/s41467-018-04342-1 apa: Morri, M., Sanchez-Romero, I., Tichy, A.-M., Kainrath, S., Gerrard, E. J., Hirschfeld, P., … Janovjak, H. L. (2018). Optical functionalization of human class A orphan G-protein-coupled receptors. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-018-04342-1 chicago: Morri, Maurizio, Inmaculada Sanchez-Romero, Alexandra-Madelaine Tichy, Stephanie Kainrath, Elliot J. Gerrard, Priscila Hirschfeld, Jan Schwarz, and Harald L Janovjak. “Optical Functionalization of Human Class A Orphan G-Protein-Coupled Receptors.” Nature Communications. Springer Nature, 2018. https://doi.org/10.1038/s41467-018-04342-1. ieee: M. Morri et al., “Optical functionalization of human class A orphan G-protein-coupled receptors,” Nature Communications, vol. 9, no. 1. Springer Nature, 2018. ista: Morri M, Sanchez-Romero I, Tichy A-M, Kainrath S, Gerrard EJ, Hirschfeld P, Schwarz J, Janovjak HL. 2018. Optical functionalization of human class A orphan G-protein-coupled receptors. Nature Communications. 9(1), 1950. mla: Morri, Maurizio, et al. “Optical Functionalization of Human Class A Orphan G-Protein-Coupled Receptors.” Nature Communications, vol. 9, no. 1, 1950, Springer Nature, 2018, doi:10.1038/s41467-018-04342-1. short: M. Morri, I. Sanchez-Romero, A.-M. Tichy, S. Kainrath, E.J. Gerrard, P. Hirschfeld, J. Schwarz, H.L. Janovjak, Nature Communications 9 (2018). date_created: 2019-02-14T10:50:24Z date_published: 2018-12-01T00:00:00Z date_updated: 2023-09-19T14:29:32Z day: '01' ddc: - '570' department: - _id: HaJa - _id: CaGu - _id: MiSi doi: 10.1038/s41467-018-04342-1 ec_funded: 1 external_id: isi: - '000432280000006' file: - access_level: open_access checksum: 8325fcc194264af4749e662a73bf66b5 content_type: application/pdf creator: kschuh date_created: 2019-02-14T10:58:29Z date_updated: 2020-07-14T12:47:14Z file_id: '5985' file_name: 2018_Springer_Morri.pdf file_size: 1349914 relation: main_file file_date_updated: 2020-07-14T12:47:14Z has_accepted_license: '1' intvolume: ' 9' isi: 1 issue: '1' language: - iso: eng month: '12' oa: 1 oa_version: Published Version project: - _id: 25548C20-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '303564' name: Microbial Ion Channels for Synthetic Neurobiology - _id: 255A6082-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: W1232-B24 name: Molecular Drug Targets publication: Nature Communications publication_identifier: issn: - 2041-1723 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Optical functionalization of human class A orphan G-protein-coupled receptors tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 9 year: '2018' ... --- _id: '5992' abstract: - lang: eng text: Lamellipodia are flat membrane protrusions formed during mesenchymal motion. Polymerization at the leading edge assembles the actin filament network and generates protrusion force. How this force is supported by the network and how the assembly rate is shared between protrusion and network retrograde flow determines the protrusion rate. We use mathematical modeling to understand experiments changing the F-actin density in lamellipodia of B16-F1 melanoma cells by modulation of Arp2/3 complex activity or knockout of the formins FMNL2 and FMNL3. Cells respond to a reduction of density with a decrease of protrusion velocity, an increase in the ratio of force to filament number, but constant network assembly rate. The relation between protrusion force and tension gradient in the F-actin network and the density dependency of friction, elasticity, and viscosity of the network explain the experimental observations. The formins act as filament nucleators and elongators with differential rates. Modulation of their activity suggests an effect on network assembly rate. Contrary to these expectations, the effect of changes in elongator composition is much weaker than the consequences of the density change. We conclude that the force acting on the leading edge membrane is the force required to drive F-actin network retrograde flow. article_processing_charge: No author: - first_name: Setareh full_name: Dolati, Setareh last_name: Dolati - first_name: Frieda full_name: Kage, Frieda last_name: Kage - first_name: Jan full_name: Mueller, Jan last_name: Mueller - first_name: Mathias full_name: Müsken, Mathias last_name: Müsken - first_name: Marieluise full_name: Kirchner, Marieluise last_name: Kirchner - first_name: Gunnar full_name: Dittmar, Gunnar last_name: Dittmar - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner - first_name: Martin full_name: Falcke, Martin last_name: Falcke citation: ama: Dolati S, Kage F, Mueller J, et al. On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility. Molecular Biology of the Cell. 2018;29(22):2674-2686. doi:10.1091/mbc.e18-02-0082 apa: Dolati, S., Kage, F., Mueller, J., Müsken, M., Kirchner, M., Dittmar, G., … Falcke, M. (2018). On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility. Molecular Biology of the Cell. American Society for Cell Biology . https://doi.org/10.1091/mbc.e18-02-0082 chicago: Dolati, Setareh, Frieda Kage, Jan Mueller, Mathias Müsken, Marieluise Kirchner, Gunnar Dittmar, Michael K Sixt, Klemens Rottner, and Martin Falcke. “On the Relation between Filament Density, Force Generation, and Protrusion Rate in Mesenchymal Cell Motility.” Molecular Biology of the Cell. American Society for Cell Biology , 2018. https://doi.org/10.1091/mbc.e18-02-0082. ieee: S. Dolati et al., “On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility,” Molecular Biology of the Cell, vol. 29, no. 22. American Society for Cell Biology , pp. 2674–2686, 2018. ista: Dolati S, Kage F, Mueller J, Müsken M, Kirchner M, Dittmar G, Sixt MK, Rottner K, Falcke M. 2018. On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility. Molecular Biology of the Cell. 29(22), 2674–2686. mla: Dolati, Setareh, et al. “On the Relation between Filament Density, Force Generation, and Protrusion Rate in Mesenchymal Cell Motility.” Molecular Biology of the Cell, vol. 29, no. 22, American Society for Cell Biology , 2018, pp. 2674–86, doi:10.1091/mbc.e18-02-0082. short: S. Dolati, F. Kage, J. Mueller, M. Müsken, M. Kirchner, G. Dittmar, M.K. Sixt, K. Rottner, M. Falcke, Molecular Biology of the Cell 29 (2018) 2674–2686. date_created: 2019-02-14T12:25:47Z date_published: 2018-11-01T00:00:00Z date_updated: 2023-09-19T14:30:23Z day: '01' ddc: - '570' department: - _id: MiSi doi: 10.1091/mbc.e18-02-0082 external_id: isi: - '000455641000011' pmid: - '30156465' file: - access_level: open_access checksum: e98465b4416b3e804c47f40086932af2 content_type: application/pdf creator: kschuh date_created: 2019-02-14T12:34:29Z date_updated: 2020-07-14T12:47:15Z file_id: '5994' file_name: 2018_ASCB_Dolati.pdf file_size: 6668971 relation: main_file file_date_updated: 2020-07-14T12:47:15Z has_accepted_license: '1' intvolume: ' 29' isi: 1 issue: '22' language: - iso: eng month: '11' oa: 1 oa_version: Published Version page: 2674-2686 pmid: 1 publication: Molecular Biology of the Cell publication_identifier: eissn: - 1939-4586 publication_status: published publisher: 'American Society for Cell Biology ' quality_controlled: '1' scopus_import: '1' status: public title: On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 29 year: '2018' ... --- _id: '6497' abstract: - lang: eng text: T cells are actively scanning pMHC-presenting cells in lymphoid organs and nonlymphoid tissues (NLTs) with divergent topologies and confinement. How the T cell actomyosin cytoskeleton facilitates this task in distinct environments is incompletely understood. Here, we show that lack of Myosin IXb (Myo9b), a negative regulator of the small GTPase Rho, led to increased Rho-GTP levels and cell surface stiffness in primary T cells. Nonetheless, intravital imaging revealed robust motility of Myo9b−/− CD8+ T cells in lymphoid tissue and similar expansion and differentiation during immune responses. In contrast, accumulation of Myo9b−/− CD8+ T cells in NLTs was strongly impaired. Specifically, Myo9b was required for T cell crossing of basement membranes, such as those which are present between dermis and epidermis. As consequence, Myo9b−/− CD8+ T cells showed impaired control of skin infections. In sum, we show that Myo9b is critical for the CD8+ T cell adaptation from lymphoid to NLT surveillance and the establishment of protective tissue–resident T cell populations. article_processing_charge: No author: - first_name: Federica full_name: Moalli, Federica last_name: Moalli - first_name: Xenia full_name: Ficht, Xenia last_name: Ficht - first_name: Philipp full_name: Germann, Philipp last_name: Germann - first_name: Mykhailo full_name: Vladymyrov, Mykhailo last_name: Vladymyrov - first_name: Bettina full_name: Stolp, Bettina last_name: Stolp - first_name: Ingrid full_name: de Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: de Vries - first_name: Ruth full_name: Lyck, Ruth last_name: Lyck - first_name: Jasmin full_name: Balmer, Jasmin last_name: Balmer - first_name: Amleto full_name: Fiocchi, Amleto last_name: Fiocchi - first_name: Mario full_name: Kreutzfeldt, Mario last_name: Kreutzfeldt - first_name: Doron full_name: Merkler, Doron last_name: Merkler - first_name: Matteo full_name: Iannacone, Matteo last_name: Iannacone - first_name: Akitaka full_name: Ariga, Akitaka last_name: Ariga - first_name: Michael H. full_name: Stoffel, Michael H. last_name: Stoffel - first_name: James full_name: Sharpe, James last_name: Sharpe - first_name: Martin full_name: Bähler, Martin last_name: Bähler - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Alba full_name: Diz-Muñoz, Alba last_name: Diz-Muñoz - first_name: Jens V. full_name: Stein, Jens V. last_name: Stein citation: ama: Moalli F, Ficht X, Germann P, et al. The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. The Journal of Experimental Medicine. 2018;2015(7):1869–1890. doi:10.1084/jem.20170896 apa: Moalli, F., Ficht, X., Germann, P., Vladymyrov, M., Stolp, B., de Vries, I., … Stein, J. V. (2018). The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. The Journal of Experimental Medicine. Rockefeller University Press. https://doi.org/10.1084/jem.20170896 chicago: Moalli, Federica, Xenia Ficht, Philipp Germann, Mykhailo Vladymyrov, Bettina Stolp, Ingrid de Vries, Ruth Lyck, et al. “The Rho Regulator Myosin IXb Enables Nonlymphoid Tissue Seeding of Protective CD8+T Cells.” The Journal of Experimental Medicine. Rockefeller University Press, 2018. https://doi.org/10.1084/jem.20170896. ieee: F. Moalli et al., “The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells,” The Journal of Experimental Medicine, vol. 2015, no. 7. Rockefeller University Press, pp. 1869–1890, 2018. ista: Moalli F, Ficht X, Germann P, Vladymyrov M, Stolp B, de Vries I, Lyck R, Balmer J, Fiocchi A, Kreutzfeldt M, Merkler D, Iannacone M, Ariga A, Stoffel MH, Sharpe J, Bähler M, Sixt MK, Diz-Muñoz A, Stein JV. 2018. The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. The Journal of Experimental Medicine. 2015(7), 1869–1890. mla: Moalli, Federica, et al. “The Rho Regulator Myosin IXb Enables Nonlymphoid Tissue Seeding of Protective CD8+T Cells.” The Journal of Experimental Medicine, vol. 2015, no. 7, Rockefeller University Press, 2018, pp. 1869–1890, doi:10.1084/jem.20170896. short: F. Moalli, X. Ficht, P. Germann, M. Vladymyrov, B. Stolp, I. de Vries, R. Lyck, J. Balmer, A. Fiocchi, M. Kreutzfeldt, D. Merkler, M. Iannacone, A. Ariga, M.H. Stoffel, J. Sharpe, M. Bähler, M.K. Sixt, A. Diz-Muñoz, J.V. Stein, The Journal of Experimental Medicine 2015 (2018) 1869–1890. date_created: 2019-05-28T12:36:47Z date_published: 2018-06-06T00:00:00Z date_updated: 2023-09-19T14:52:08Z day: '06' ddc: - '570' department: - _id: MiSi doi: 10.1084/jem.20170896 external_id: isi: - '000440822900011' file: - access_level: open_access checksum: 86ae5331f9bfced9a6358a790a04bef4 content_type: application/pdf creator: kschuh date_created: 2019-05-28T12:40:05Z date_updated: 2020-07-14T12:47:32Z file_id: '6498' file_name: 2018_rupress_Moalli.pdf file_size: 3841660 relation: main_file file_date_updated: 2020-07-14T12:47:32Z has_accepted_license: '1' intvolume: ' 2015' isi: 1 issue: '7' language: - iso: eng month: '06' oa: 1 oa_version: Published Version page: 1869–1890 publication: The Journal of Experimental Medicine publication_identifier: eissn: - 1540-9538 issn: - 0022-1007 publication_status: published publisher: Rockefeller University Press quality_controlled: '1' scopus_import: '1' status: public title: The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 2015 year: '2018' ... --- _id: '402' abstract: - lang: eng text: During metastasis, malignant cells escape the primary tumor, intravasate lymphatic vessels, and reach draining sentinel lymph nodes before they colonize distant organs via the blood circulation. Although lymph node metastasis in cancer patients correlates with poor prognosis, evidence is lacking as to whether and how tumor cells enter the bloodstream via lymph nodes. To investigate this question, we delivered carcinoma cells into the lymph nodes of mice by microinfusing the cells into afferent lymphatic vessels. We found that tumor cells rapidly infiltrated the lymph node parenchyma, invaded blood vessels, and seeded lung metastases without involvement of the thoracic duct. These results suggest that the lymph node blood vessels can serve as an exit route for systemic dissemination of cancer cells in experimental mouse models. Whether this form of tumor cell spreading occurs in cancer patients remains to be determined. acknowledged_ssus: - _id: Bio acknowledgement: "M.B. was supported by the Cell Communication in Health and Disease graduate study program of the Austrian Science Fund (FWF) and the Medical University of Vienna. M.S. was supported by the European Research Council (grant ERC GA 281556) and an FWF START award.\r\nWe thank C. Moussion for establishing the intralymphatic injection at IST Austria and for providing anti-PNAd hybridoma supernatant, R. Förster and A. Braun for sharing the intralymphatic injection technology, K. Vaahtomeri for the lentiviral constructs, M. Hons for establishing in vivo multiphoton imaging, the Sixt lab for intellectual input, M. Schunn for help with the design of the in vivo experiments, F. Langer for technical assistance with the in vivo experiments, the bioimaging facility of IST Austria for support, and R. Efferl for providing the CT26 cell line." article_processing_charge: No article_type: original author: - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Frank P full_name: Assen, Frank P id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87 last_name: Assen orcid: 0000-0003-3470-6119 - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Jun full_name: Abe, Jun last_name: Abe - first_name: Helga full_name: Schachner, Helga last_name: Schachner - first_name: Gabriele full_name: Asfour, Gabriele last_name: Asfour - first_name: Zsuzsanna full_name: Bagó Horváth, Zsuzsanna last_name: Bagó Horváth - first_name: Jens full_name: Stein, Jens last_name: Stein - first_name: Pavel full_name: Uhrin, Pavel last_name: Uhrin - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki citation: ama: Brown M, Assen FP, Leithner AF, et al. Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. Science. 2018;359(6382):1408-1411. doi:10.1126/science.aal3662 apa: Brown, M., Assen, F. P., Leithner, A. F., Abe, J., Schachner, H., Asfour, G., … Kerjaschki, D. (2018). Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.aal3662 chicago: Brown, Markus, Frank P Assen, Alexander F Leithner, Jun Abe, Helga Schachner, Gabriele Asfour, Zsuzsanna Bagó Horváth, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” Science. American Association for the Advancement of Science, 2018. https://doi.org/10.1126/science.aal3662. ieee: M. Brown et al., “Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice,” Science, vol. 359, no. 6382. American Association for the Advancement of Science, pp. 1408–1411, 2018. ista: Brown M, Assen FP, Leithner AF, Abe J, Schachner H, Asfour G, Bagó Horváth Z, Stein J, Uhrin P, Sixt MK, Kerjaschki D. 2018. Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. Science. 359(6382), 1408–1411. mla: Brown, Markus, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” Science, vol. 359, no. 6382, American Association for the Advancement of Science, 2018, pp. 1408–11, doi:10.1126/science.aal3662. short: M. Brown, F.P. Assen, A.F. Leithner, J. Abe, H. Schachner, G. Asfour, Z. Bagó Horváth, J. Stein, P. Uhrin, M.K. Sixt, D. Kerjaschki, Science 359 (2018) 1408–1411. date_created: 2018-12-11T11:46:16Z date_published: 2018-03-23T00:00:00Z date_updated: 2024-03-27T23:30:09Z day: '23' department: - _id: MiSi doi: 10.1126/science.aal3662 ec_funded: 1 external_id: isi: - '000428043600047' pmid: - '29567714' intvolume: ' 359' isi: 1 issue: '6382' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1126/science.aal3662 month: '03' oa: 1 oa_version: Published Version page: 1408 - 1411 pmid: 1 project: - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Science publication_status: published publisher: American Association for the Advancement of Science publist_id: '7428' quality_controlled: '1' related_material: record: - id: '6947' relation: dissertation_contains status: public scopus_import: '1' status: public title: Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 359 year: '2018' ... --- _id: '323' abstract: - lang: eng text: 'In the here presented thesis, we explore the role of branched actin networks in cell migration and antigen presentation, the two most relevant processes in dendritic cell biology. Branched actin networks construct lamellipodial protrusions at the leading edge of migrating cells. These are typically seen as adhesive structures, which mediate force transduction to the extracellular matrix that leads to forward locomotion. We ablated Arp2/3 nucleation promoting factor WAVE in DCs and found that the resulting cells lack lamellipodial protrusions. Instead, depending on the maturation state, one or multiple filopodia were formed. By challenging these cells in a variety of migration assays we found that lamellipodial protrusions are dispensable for the locomotion of leukocytes and actually dampen the speed of migration. However, lamellipodia are critically required to negotiate complex environments that DCs experience while they travel to the next draining lymph node. Taken together our results suggest that leukocyte lamellipodia have rather a sensory- than a force transducing function. Furthermore, we show for the first time structure and dynamics of dendritic cell F-actin at the immunological synapse with naïve T cells. Dendritic cell F-actin appears as dynamic foci that are nucleated by the Arp2/3 complex. WAVE ablated dendritic cells show increased membrane tension, leading to an altered ultrastructure of the immunological synapse and severe T cell priming defects. These results point towards a previously unappreciated role of the cellular mechanics of dendritic cells in T cell activation. Additionally, we present a novel cell culture based system for the differentiation of dendritic cells from conditionally immortalized hematopoietic precursors. These precursor cells are genetically tractable via the CRISPR/Cas9 system while they retain their ability to differentiate into highly migratory dendritic cells and other immune cells. This will foster the study of all aspects of dendritic cell biology and beyond. ' acknowledged_ssus: - _id: NanoFab - _id: Bio - _id: PreCl - _id: EM-Fac acknowledgement: "First of all I would like to thank Michael Sixt for giving me the opportunity to work in \r\nhis group and for his support throughout the years. He is a truly inspiring person and \r\nthe best boss one can imagine. I would \ also like to thank all current and past \r\nmembers of the Sixt group for their help and the great working atmosphere in the lab. \r\nIt is a true privilege to work with such a bright, funny and friendly group of people and \r\nI’m proud \ that I could be part of it. Furthermore, I would like to say ‘thank \ you’ to Daria Siekhaus for all the meetings and discussion we had throughout the years \r\nand to Federica Benvenuti for being part of my committee. \ I am also grateful to Jack \r\nMerrin in the nanofabrication facility \ and all the people working in the bioimaging-\r\n, the electron microscopy- and the preclinical facilities." alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X citation: ama: Leithner AF. Branched actin networks in dendritic cell biology. 2018. doi:10.15479/AT:ISTA:th_998 apa: Leithner, A. F. (2018). Branched actin networks in dendritic cell biology. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_998 chicago: Leithner, Alexander F. “Branched Actin Networks in Dendritic Cell Biology.” Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th_998. ieee: A. F. Leithner, “Branched actin networks in dendritic cell biology,” Institute of Science and Technology Austria, 2018. ista: Leithner AF. 2018. Branched actin networks in dendritic cell biology. Institute of Science and Technology Austria. mla: Leithner, Alexander F. Branched Actin Networks in Dendritic Cell Biology. Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th_998. short: A.F. Leithner, Branched Actin Networks in Dendritic Cell Biology, Institute of Science and Technology Austria, 2018. date_created: 2018-12-11T11:45:49Z date_published: 2018-04-12T00:00:00Z date_updated: 2023-09-07T12:39:44Z day: '12' ddc: - '571' - '599' - '610' degree_awarded: PhD department: - _id: MiSi doi: 10.15479/AT:ISTA:th_998 file: - access_level: closed checksum: d5e3edbac548c26c1fa43a4b37a54a4c content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document creator: dernst date_created: 2019-04-05T09:23:11Z date_updated: 2021-02-11T23:30:17Z embargo_to: open_access file_id: '6219' file_name: PhD_thesis_AlexLeithner_final_version.docx file_size: 29027671 relation: source_file - access_level: open_access checksum: 071f7476db29e41146824ebd0697cb10 content_type: application/pdf creator: dernst date_created: 2019-04-05T09:23:11Z date_updated: 2021-02-11T11:17:16Z embargo: 2019-04-15 file_id: '6220' file_name: PhD_thesis_AlexLeithner.pdf file_size: 66045341 relation: main_file file_date_updated: 2021-02-11T23:30:17Z has_accepted_license: '1' language: - iso: eng month: '04' oa: 1 oa_version: Published Version page: '99' publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria publist_id: '7542' pubrep_id: '998' related_material: record: - id: '1321' relation: part_of_dissertation status: public status: public supervisor: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 title: Branched actin networks in dendritic cell biology tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: dissertation user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 year: '2018' ... --- _id: '15' abstract: - lang: eng text: Although much is known about the physiological framework of T cell motility, and numerous rate-limiting molecules have been identified through loss-of-function approaches, an integrated functional concept of T cell motility is lacking. Here, we used in vivo precision morphometry together with analysis of cytoskeletal dynamics in vitro to deconstruct the basic mechanisms of T cell migration within lymphatic organs. We show that the contributions of the integrin LFA-1 and the chemokine receptor CCR7 are complementary rather than positioned in a linear pathway, as they are during leukocyte extravasation from the blood vasculature. Our data demonstrate that CCR7 controls cortical actin flows, whereas integrins mediate substrate friction that is sufficient to drive locomotion in the absence of considerable surface adhesions and plasma membrane flux. acknowledged_ssus: - _id: SSU acknowledgement: This work was funded by grants from the European Research Council (ERC StG 281556 and CoG 724373) and the Austrian Science Foundation (FWF) to M.S. and by Swiss National Foundation (SNF) project grants 31003A_135649, 31003A_153457 and CR23I3_156234 to J.V.S. F.G. received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 747687, and J.R. was funded by an EMBO long-term fellowship (ALTF 1396-2014). article_processing_charge: No author: - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Florian R full_name: Gärtner, Florian R id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 - first_name: Jun full_name: Abe, Jun last_name: Abe - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Jens full_name: Stein, Jens last_name: Stein - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Hons M, Kopf A, Hauschild R, et al. Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. Nature Immunology. 2018;19(6):606-616. doi:10.1038/s41590-018-0109-z apa: Hons, M., Kopf, A., Hauschild, R., Leithner, A. F., Gärtner, F. R., Abe, J., … Sixt, M. K. (2018). Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/s41590-018-0109-z chicago: Hons, Miroslav, Aglaja Kopf, Robert Hauschild, Alexander F Leithner, Florian R Gärtner, Jun Abe, Jörg Renkawitz, Jens Stein, and Michael K Sixt. “Chemokines and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal Migration of T Cells.” Nature Immunology. Nature Publishing Group, 2018. https://doi.org/10.1038/s41590-018-0109-z. ieee: M. Hons et al., “Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells,” Nature Immunology, vol. 19, no. 6. Nature Publishing Group, pp. 606–616, 2018. ista: Hons M, Kopf A, Hauschild R, Leithner AF, Gärtner FR, Abe J, Renkawitz J, Stein J, Sixt MK. 2018. Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. Nature Immunology. 19(6), 606–616. mla: Hons, Miroslav, et al. “Chemokines and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal Migration of T Cells.” Nature Immunology, vol. 19, no. 6, Nature Publishing Group, 2018, pp. 606–16, doi:10.1038/s41590-018-0109-z. short: M. Hons, A. Kopf, R. Hauschild, A.F. Leithner, F.R. Gärtner, J. Abe, J. Renkawitz, J. Stein, M.K. Sixt, Nature Immunology 19 (2018) 606–616. date_created: 2018-12-11T11:44:10Z date_published: 2018-05-18T00:00:00Z date_updated: 2024-03-27T23:30:39Z day: '18' department: - _id: MiSi - _id: Bio doi: 10.1038/s41590-018-0109-z ec_funded: 1 external_id: isi: - '000433041500026' pmid: - '29777221' intvolume: ' 19' isi: 1 issue: '6' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pubmed/29777221 month: '05' oa: 1 oa_version: Published Version page: 606 - 616 pmid: 1 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 260AA4E2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '747687' name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells - _id: 25A48D24-B435-11E9-9278-68D0E5697425 grant_number: ALTF 1396-2014 name: Molecular and system level view of immune cell migration - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Nature Immunology publication_status: published publisher: Nature Publishing Group publist_id: '8040' quality_controlled: '1' related_material: record: - id: '6891' relation: dissertation_contains status: public scopus_import: '1' status: public title: Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 19 year: '2018' ... --- _id: '569' abstract: - lang: eng text: The actomyosin ring generates force to ingress the cytokinetic cleavage furrow in animal cells, yet its filament organization and the mechanism of contractility is not well understood. We quantified actin filament order in human cells using fluorescence polarization microscopy and found that cleavage furrow ingression initiates by contraction of an equatorial actin network with randomly oriented filaments. The network subsequently gradually reoriented actin filaments along the cell equator. This strictly depended on myosin II activity, suggesting local network reorganization by mechanical forces. Cortical laser microsurgery revealed that during cytokinesis progression, mechanical tension increased substantially along the direction of the cell equator, while the network contracted laterally along the pole-to-pole axis without a detectable increase in tension. Our data suggest that an asymmetric increase in cortical tension promotes filament reorientation along the cytokinetic cleavage furrow, which might have implications for diverse other biological processes involving actomyosin rings. article_number: e30867 author: - first_name: Felix full_name: Spira, Felix last_name: Spira - first_name: Sara full_name: Cuylen Haering, Sara last_name: Cuylen Haering - first_name: Shalin full_name: Mehta, Shalin last_name: Mehta - first_name: Matthias full_name: Samwer, Matthias last_name: Samwer - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Amitabh full_name: Verma, Amitabh last_name: Verma - first_name: Rudolf full_name: Oldenbourg, Rudolf last_name: Oldenbourg - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Daniel full_name: Gerlich, Daniel last_name: Gerlich citation: ama: Spira F, Cuylen Haering S, Mehta S, et al. Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. eLife. 2017;6. doi:10.7554/eLife.30867 apa: Spira, F., Cuylen Haering, S., Mehta, S., Samwer, M., Reversat, A., Verma, A., … Gerlich, D. (2017). Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.30867 chicago: Spira, Felix, Sara Cuylen Haering, Shalin Mehta, Matthias Samwer, Anne Reversat, Amitabh Verma, Rudolf Oldenbourg, Michael K Sixt, and Daniel Gerlich. “Cytokinesis in Vertebrate Cells Initiates by Contraction of an Equatorial Actomyosin Network Composed of Randomly Oriented Filaments.” ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.30867. ieee: F. Spira et al., “Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments,” eLife, vol. 6. eLife Sciences Publications, 2017. ista: Spira F, Cuylen Haering S, Mehta S, Samwer M, Reversat A, Verma A, Oldenbourg R, Sixt MK, Gerlich D. 2017. Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. eLife. 6, e30867. mla: Spira, Felix, et al. “Cytokinesis in Vertebrate Cells Initiates by Contraction of an Equatorial Actomyosin Network Composed of Randomly Oriented Filaments.” ELife, vol. 6, e30867, eLife Sciences Publications, 2017, doi:10.7554/eLife.30867. short: F. Spira, S. Cuylen Haering, S. Mehta, M. Samwer, A. Reversat, A. Verma, R. Oldenbourg, M.K. Sixt, D. Gerlich, ELife 6 (2017). date_created: 2018-12-11T11:47:14Z date_published: 2017-11-06T00:00:00Z date_updated: 2023-02-23T12:30:29Z day: '06' ddc: - '570' department: - _id: MiSi doi: 10.7554/eLife.30867 file: - access_level: open_access checksum: ba09c1451153d39e4f4b7cee013e314c content_type: application/pdf creator: system date_created: 2018-12-12T10:10:40Z date_updated: 2020-07-14T12:47:10Z file_id: '4829' file_name: IST-2017-919-v1+1_elife-30867-figures-v1.pdf file_size: 9666973 relation: main_file - access_level: open_access checksum: 01eb51f1d6ad679947415a51c988e137 content_type: application/pdf creator: system date_created: 2018-12-12T10:10:41Z date_updated: 2020-07-14T12:47:10Z file_id: '4830' file_name: IST-2017-919-v1+2_elife-30867-v1.pdf file_size: 5951246 relation: main_file file_date_updated: 2020-07-14T12:47:10Z has_accepted_license: '1' intvolume: ' 6' language: - iso: eng month: '11' oa: 1 oa_version: Published Version publication: eLife publication_identifier: issn: - 2050084X publication_status: published publisher: eLife Sciences Publications publist_id: '7245' pubrep_id: '919' quality_controlled: '1' scopus_import: 1 status: public title: Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 6 year: '2017' ... --- _id: '571' abstract: - lang: eng text: Blood platelets are critical for hemostasis and thrombosis and play diverse roles during immune responses. Despite these versatile tasks in mammalian biology, their skills on a cellular level are deemed limited, mainly consisting in rolling, adhesion, and aggregate formation. Here, we identify an unappreciated asset of platelets and show that adherent platelets use adhesion receptors to mechanically probe the adhesive substrate in their local microenvironment. When actomyosin-dependent traction forces overcome substrate resistance, platelets migrate and pile up the adhesive substrate together with any bound particulate material. They use this ability to act as cellular scavengers, scanning the vascular surface for potential invaders and collecting deposited bacteria. Microbe collection by migrating platelets boosts the activity of professional phagocytes, exacerbating inflammatory tissue injury in sepsis. This assigns platelets a central role in innate immune responses and identifies them as potential targets to dampen inflammatory tissue damage in clinical scenarios of severe systemic infection. In addition to their role in thrombosis and hemostasis, platelets can also migrate to sites of infection to help trap bacteria and clear the vascular surface. author: - first_name: Florian R full_name: Gärtner, Florian R id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 - first_name: Zerkah full_name: Ahmad, Zerkah last_name: Ahmad - first_name: Gerhild full_name: Rosenberger, Gerhild last_name: Rosenberger - first_name: Shuxia full_name: Fan, Shuxia last_name: Fan - first_name: Leo full_name: Nicolai, Leo last_name: Nicolai - first_name: Benjamin full_name: Busch, Benjamin last_name: Busch - first_name: Gökce full_name: Yavuz, Gökce last_name: Yavuz - first_name: Manja full_name: Luckner, Manja last_name: Luckner - first_name: Hellen full_name: Ishikawa Ankerhold, Hellen last_name: Ishikawa Ankerhold - first_name: Roman full_name: Hennel, Roman last_name: Hennel - first_name: Alexandre full_name: Benechet, Alexandre last_name: Benechet - first_name: Michael full_name: Lorenz, Michael last_name: Lorenz - first_name: Sue full_name: Chandraratne, Sue last_name: Chandraratne - first_name: Irene full_name: Schubert, Irene last_name: Schubert - first_name: Sebastian full_name: Helmer, Sebastian last_name: Helmer - first_name: Bianca full_name: Striednig, Bianca last_name: Striednig - first_name: Konstantin full_name: Stark, Konstantin last_name: Stark - first_name: Marek full_name: Janko, Marek last_name: Janko - first_name: Ralph full_name: Böttcher, Ralph last_name: Böttcher - first_name: Admar full_name: Verschoor, Admar last_name: Verschoor - first_name: Catherine full_name: Leon, Catherine last_name: Leon - first_name: Christian full_name: Gachet, Christian last_name: Gachet - first_name: Thomas full_name: Gudermann, Thomas last_name: Gudermann - first_name: Michael full_name: Mederos Y Schnitzler, Michael last_name: Mederos Y Schnitzler - first_name: Zachary full_name: Pincus, Zachary last_name: Pincus - first_name: Matteo full_name: Iannacone, Matteo last_name: Iannacone - first_name: Rainer full_name: Haas, Rainer last_name: Haas - first_name: Gerhard full_name: Wanner, Gerhard last_name: Wanner - first_name: Kirsten full_name: Lauber, Kirsten last_name: Lauber - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Steffen full_name: Massberg, Steffen last_name: Massberg citation: ama: Gärtner FR, Ahmad Z, Rosenberger G, et al. Migrating platelets are mechano scavengers that collect and bundle bacteria. Cell Press. 2017;171(6):1368-1382. doi:10.1016/j.cell.2017.11.001 apa: Gärtner, F. R., Ahmad, Z., Rosenberger, G., Fan, S., Nicolai, L., Busch, B., … Massberg, S. (2017). Migrating platelets are mechano scavengers that collect and bundle bacteria. Cell Press. Cell Press. https://doi.org/10.1016/j.cell.2017.11.001 chicago: Gärtner, Florian R, Zerkah Ahmad, Gerhild Rosenberger, Shuxia Fan, Leo Nicolai, Benjamin Busch, Gökce Yavuz, et al. “Migrating Platelets Are Mechano Scavengers That Collect and Bundle Bacteria.” Cell Press. Cell Press, 2017. https://doi.org/10.1016/j.cell.2017.11.001. ieee: F. R. Gärtner et al., “Migrating platelets are mechano scavengers that collect and bundle bacteria,” Cell Press, vol. 171, no. 6. Cell Press, pp. 1368–1382, 2017. ista: Gärtner FR, Ahmad Z, Rosenberger G, Fan S, Nicolai L, Busch B, Yavuz G, Luckner M, Ishikawa Ankerhold H, Hennel R, Benechet A, Lorenz M, Chandraratne S, Schubert I, Helmer S, Striednig B, Stark K, Janko M, Böttcher R, Verschoor A, Leon C, Gachet C, Gudermann T, Mederos Y Schnitzler M, Pincus Z, Iannacone M, Haas R, Wanner G, Lauber K, Sixt MK, Massberg S. 2017. Migrating platelets are mechano scavengers that collect and bundle bacteria. Cell Press. 171(6), 1368–1382. mla: Gärtner, Florian R., et al. “Migrating Platelets Are Mechano Scavengers That Collect and Bundle Bacteria.” Cell Press, vol. 171, no. 6, Cell Press, 2017, pp. 1368–82, doi:10.1016/j.cell.2017.11.001. short: F.R. Gärtner, Z. Ahmad, G. Rosenberger, S. Fan, L. Nicolai, B. Busch, G. Yavuz, M. Luckner, H. Ishikawa Ankerhold, R. Hennel, A. Benechet, M. Lorenz, S. Chandraratne, I. Schubert, S. Helmer, B. Striednig, K. Stark, M. Janko, R. Böttcher, A. Verschoor, C. Leon, C. Gachet, T. Gudermann, M. Mederos Y Schnitzler, Z. Pincus, M. Iannacone, R. Haas, G. Wanner, K. Lauber, M.K. Sixt, S. Massberg, Cell Press 171 (2017) 1368–1382. date_created: 2018-12-11T11:47:15Z date_published: 2017-11-30T00:00:00Z date_updated: 2021-01-12T08:03:15Z day: '30' department: - _id: MiSi doi: 10.1016/j.cell.2017.11.001 ec_funded: 1 intvolume: ' 171' issue: '6' language: - iso: eng month: '11' oa_version: None page: 1368 - 1382 project: - _id: 260AA4E2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '747687' name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells publication: Cell Press publication_identifier: issn: - '00928674' publication_status: published publisher: Cell Press publist_id: '7243' quality_controlled: '1' scopus_import: 1 status: public title: Migrating platelets are mechano scavengers that collect and bundle bacteria type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 171 year: '2017' ... --- _id: '659' abstract: - lang: eng text: Migration frequently involves Rac-mediated protrusion of lamellipodia, formed by Arp2/3 complex-dependent branching thought to be crucial for force generation and stability of these networks. The formins FMNL2 and FMNL3 are Cdc42 effectors targeting to the lamellipodium tip and shown here to nucleate and elongate actin filaments with complementary activities in vitro. In migrating B16-F1 melanoma cells, both formins contribute to the velocity of lamellipodium protrusion. Loss of FMNL2/3 function in melanoma cells and fibroblasts reduces lamellipodial width, actin filament density and -bundling, without changing patterns of Arp2/3 complex incorporation. Strikingly, in melanoma cells, FMNL2/3 gene inactivation almost completely abolishes protrusion forces exerted by lamellipodia and modifies their ultrastructural organization. Consistently, CRISPR/Cas-mediated depletion of FMNL2/3 in fibroblasts reduces both migration and capability of cells to move against viscous media. Together, we conclude that force generation in lamellipodia strongly depends on FMNL formin activity, operating in addition to Arp2/3 complex-dependent filament branching. article_number: '14832' article_processing_charge: No author: - first_name: Frieda full_name: Kage, Frieda last_name: Kage - first_name: Moritz full_name: Winterhoff, Moritz last_name: Winterhoff - first_name: Vanessa full_name: Dimchev, Vanessa last_name: Dimchev - first_name: Jan full_name: Müller, Jan id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D last_name: Müller - first_name: Tobias full_name: Thalheim, Tobias last_name: Thalheim - first_name: Anika full_name: Freise, Anika last_name: Freise - first_name: Stefan full_name: Brühmann, Stefan last_name: Brühmann - first_name: Jana full_name: Kollasser, Jana last_name: Kollasser - first_name: Jennifer full_name: Block, Jennifer last_name: Block - first_name: Georgi A full_name: Dimchev, Georgi A last_name: Dimchev - first_name: Matthias full_name: Geyer, Matthias last_name: Geyer - first_name: Hams full_name: Schnittler, Hams last_name: Schnittler - first_name: Cord full_name: Brakebusch, Cord last_name: Brakebusch - first_name: Theresia full_name: Stradal, Theresia last_name: Stradal - first_name: Marie full_name: Carlier, Marie last_name: Carlier - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Josef full_name: Käs, Josef last_name: Käs - first_name: Jan full_name: Faix, Jan last_name: Faix - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner citation: ama: Kage F, Winterhoff M, Dimchev V, et al. FMNL formins boost lamellipodial force generation. Nature Communications. 2017;8. doi:10.1038/ncomms14832 apa: Kage, F., Winterhoff, M., Dimchev, V., Müller, J., Thalheim, T., Freise, A., … Rottner, K. (2017). FMNL formins boost lamellipodial force generation. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms14832 chicago: Kage, Frieda, Moritz Winterhoff, Vanessa Dimchev, Jan Müller, Tobias Thalheim, Anika Freise, Stefan Brühmann, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/ncomms14832. ieee: F. Kage et al., “FMNL formins boost lamellipodial force generation,” Nature Communications, vol. 8. Nature Publishing Group, 2017. ista: Kage F, Winterhoff M, Dimchev V, Müller J, Thalheim T, Freise A, Brühmann S, Kollasser J, Block J, Dimchev GA, Geyer M, Schnittler H, Brakebusch C, Stradal T, Carlier M, Sixt MK, Käs J, Faix J, Rottner K. 2017. FMNL formins boost lamellipodial force generation. Nature Communications. 8, 14832. mla: Kage, Frieda, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature Communications, vol. 8, 14832, Nature Publishing Group, 2017, doi:10.1038/ncomms14832. short: F. Kage, M. Winterhoff, V. Dimchev, J. Müller, T. Thalheim, A. Freise, S. Brühmann, J. Kollasser, J. Block, G.A. Dimchev, M. Geyer, H. Schnittler, C. Brakebusch, T. Stradal, M. Carlier, M.K. Sixt, J. Käs, J. Faix, K. Rottner, Nature Communications 8 (2017). date_created: 2018-12-11T11:47:46Z date_published: 2017-03-22T00:00:00Z date_updated: 2021-01-12T08:08:06Z day: '22' ddc: - '570' department: - _id: MiSi doi: 10.1038/ncomms14832 file: - access_level: open_access checksum: dae30190291c3630e8102d8714a8d23e content_type: application/pdf creator: system date_created: 2018-12-12T10:14:21Z date_updated: 2020-07-14T12:47:34Z file_id: '5072' file_name: IST-2017-902-v1+1_Kage_et_al-2017-Nature_Communications.pdf file_size: 9523746 relation: main_file file_date_updated: 2020-07-14T12:47:34Z has_accepted_license: '1' intvolume: ' 8' language: - iso: eng month: '03' oa: 1 oa_version: Published Version publication: Nature Communications publication_identifier: issn: - '20411723' publication_status: published publisher: Nature Publishing Group publist_id: '7075' pubrep_id: '902' quality_controlled: '1' scopus_import: 1 status: public title: FMNL formins boost lamellipodial force generation tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2017' ... --- _id: '668' abstract: - lang: eng text: Macrophage filopodia, finger-like membrane protrusions, were first implicated in phagocytosis more than 100 years ago, but little is still known about the involvement of these actin-dependent structures in particle clearance. Using spinning disk confocal microscopy to image filopodial dynamics in mouse resident Lifeact-EGFP macrophages, we show that filopodia, or filopodia-like structures, support pathogen clearance by multiple means. Filopodia supported the phagocytic uptake of bacterial (Escherichia coli) particles by (i) capturing along the filopodial shaft and surfing toward the cell body, the most common mode of capture; (ii) capturing via the tip followed by retraction; (iii) combinations of surfing and retraction; or (iv) sweeping actions. In addition, filopodia supported the uptake of zymosan (Saccharomyces cerevisiae) particles by (i) providing fixation, (ii) capturing at the tip and filopodia-guided actin anterograde flow with phagocytic cup formation, and (iii) the rapid growth of new protrusions. To explore the role of filopodia-inducing Cdc42, we generated myeloid-restricted Cdc42 knock-out mice. Cdc42-deficient macrophages exhibited rapid phagocytic cup kinetics, but reduced particle clearance, which could be explained by the marked rounded-up morphology of these cells. Macrophages lacking Myo10, thought to act downstream of Cdc42, had normal morphology, motility, and phagocytic cup formation, but displayed markedly reduced filopodia formation. In conclusion, live-cell imaging revealed multiple mechanisms involving macrophage filopodia in particle capture and engulfment. Cdc42 is not critical for filopodia or phagocytic cup formation, but plays a key role in driving macrophage lamellipodial spreading. article_type: original author: - first_name: Markus full_name: Horsthemke, Markus last_name: Horsthemke - first_name: Anne full_name: Bachg, Anne last_name: Bachg - first_name: Katharina full_name: Groll, Katharina last_name: Groll - first_name: Sven full_name: Moyzio, Sven last_name: Moyzio - first_name: Barbara full_name: Müther, Barbara last_name: Müther - first_name: Sandra full_name: Hemkemeyer, Sandra last_name: Hemkemeyer - first_name: Roland full_name: Wedlich Söldner, Roland last_name: Wedlich Söldner - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Sebastian full_name: Tacke, Sebastian last_name: Tacke - first_name: Martin full_name: Bähler, Martin last_name: Bähler - first_name: Peter full_name: Hanley, Peter last_name: Hanley citation: ama: Horsthemke M, Bachg A, Groll K, et al. Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. 2017;292(17):7258-7273. doi:10.1074/jbc.M116.766923 apa: Horsthemke, M., Bachg, A., Groll, K., Moyzio, S., Müther, B., Hemkemeyer, S., … Hanley, P. (2017). Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. American Society for Biochemistry and Molecular Biology. https://doi.org/10.1074/jbc.M116.766923 chicago: Horsthemke, Markus, Anne Bachg, Katharina Groll, Sven Moyzio, Barbara Müther, Sandra Hemkemeyer, Roland Wedlich Söldner, et al. “Multiple Roles of Filopodial Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal of Biological Chemistry. American Society for Biochemistry and Molecular Biology, 2017. https://doi.org/10.1074/jbc.M116.766923. ieee: M. Horsthemke et al., “Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion,” Journal of Biological Chemistry, vol. 292, no. 17. American Society for Biochemistry and Molecular Biology, pp. 7258–7273, 2017. ista: Horsthemke M, Bachg A, Groll K, Moyzio S, Müther B, Hemkemeyer S, Wedlich Söldner R, Sixt MK, Tacke S, Bähler M, Hanley P. 2017. Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. 292(17), 7258–7273. mla: Horsthemke, Markus, et al. “Multiple Roles of Filopodial Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal of Biological Chemistry, vol. 292, no. 17, American Society for Biochemistry and Molecular Biology, 2017, pp. 7258–73, doi:10.1074/jbc.M116.766923. short: M. Horsthemke, A. Bachg, K. Groll, S. Moyzio, B. Müther, S. Hemkemeyer, R. Wedlich Söldner, M.K. Sixt, S. Tacke, M. Bähler, P. Hanley, Journal of Biological Chemistry 292 (2017) 7258–7273. date_created: 2018-12-11T11:47:49Z date_published: 2017-04-28T00:00:00Z date_updated: 2021-01-12T08:08:34Z day: '28' ddc: - '570' department: - _id: MiSi doi: 10.1074/jbc.M116.766923 file: - access_level: open_access checksum: d488162874326a4bb056065fa549dc4a content_type: application/pdf creator: dernst date_created: 2019-10-24T15:25:42Z date_updated: 2020-07-14T12:47:37Z file_id: '6971' file_name: 2017_JBC_Horsthemke.pdf file_size: 5647880 relation: main_file file_date_updated: 2020-07-14T12:47:37Z has_accepted_license: '1' intvolume: ' 292' issue: '17' language: - iso: eng month: '04' oa: 1 oa_version: Published Version page: 7258 - 7273 publication: Journal of Biological Chemistry publication_identifier: issn: - '00219258' publication_status: published publisher: American Society for Biochemistry and Molecular Biology publist_id: '7059' quality_controlled: '1' scopus_import: 1 status: public title: Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 292 year: '2017' ... --- _id: '672' abstract: - lang: eng text: Trafficking cells frequently transmigrate through epithelial and endothelial monolayers. How monolayers cooperate with the penetrating cells to support their transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic capillaries as a model system for transendothelial migration. We find that the chemokine CCL21, which is the decisive guidance cue for intravasation, mainly localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes extracellularly enriched at the sites of endothelial cell-cell junctions. When we reconstitute the transmigration process in vitro, we find that secretion of CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and selective calcium chelation in lymphatic endothelium attenuates transmigration. Altogether, our data demonstrate a chemokine-mediated feedback between DCs and lymphatic endothelium, which facilitates transendothelial migration. article_processing_charge: Yes author: - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner - first_name: Matthias full_name: Mehling, Matthias id: 3C23B994-F248-11E8-B48F-1D18A9856A87 last_name: Mehling orcid: 0000-0001-8599-1226 - first_name: Walter full_name: Kaufmann, Walter id: 3F99E422-F248-11E8-B48F-1D18A9856A87 last_name: Kaufmann orcid: 0000-0001-9735-5315 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 2017;19(5):902-909. doi:10.1016/j.celrep.2017.04.027 apa: Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling, M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.027 chicago: Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.027. ieee: K. Vaahtomeri et al., “Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia,” Cell Reports, vol. 19, no. 5. Cell Press, pp. 902–909, 2017. ista: Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909. mla: Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports, vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:10.1016/j.celrep.2017.04.027. short: K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling, W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909. date_created: 2018-12-11T11:47:50Z date_published: 2017-05-02T00:00:00Z date_updated: 2023-02-23T12:50:09Z day: '02' ddc: - '570' department: - _id: MiSi - _id: Bio - _id: EM-Fac doi: 10.1016/j.celrep.2017.04.027 ec_funded: 1 file: - access_level: open_access checksum: 8fdddaab1f1d76a6ec9ca94dcb6b07a2 content_type: application/pdf creator: system date_created: 2018-12-12T10:14:54Z date_updated: 2020-07-14T12:47:38Z file_id: '5109' file_name: IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf file_size: 2248814 relation: main_file file_date_updated: 2020-07-14T12:47:38Z has_accepted_license: '1' intvolume: ' 19' issue: '5' language: - iso: eng month: '05' oa: 1 oa_version: Published Version page: 902 - 909 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Cell Reports publication_identifier: issn: - '22111247' publication_status: published publisher: Cell Press publist_id: '7052' pubrep_id: '900' quality_controlled: '1' scopus_import: 1 status: public title: Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 19 year: '2017' ... --- _id: '674' abstract: - lang: eng text: Navigation of cells along gradients of guidance cues is a determining step in many developmental and immunological processes. Gradients can either be soluble or immobilized to tissues as demonstrated for the haptotactic migration of dendritic cells (DCs) toward higher concentrations of immobilized chemokine CCL21. To elucidate how gradient characteristics govern cellular response patterns, we here introduce an in vitro system allowing to track migratory responses of DCs to precisely controlled immobilized gradients of CCL21. We find that haptotactic sensing depends on the absolute CCL21 concentration and local steepness of the gradient, consistent with a scenario where DC directionality is governed by the signal-to-noise ratio of CCL21 binding to the receptor CCR7. We find that the conditions for optimal DC guidance are perfectly provided by the CCL21 gradients we measure in vivo. Furthermore, we find that CCR7 signal termination by the G-protein-coupled receptor kinase 6 (GRK6) is crucial for haptotactic but dispensable for chemotactic CCL21 gradient sensing in vitro and confirm those observations in vivo. These findings suggest that stable, tissue-bound CCL21 gradients as sustainable “roads” ensure optimal guidance in vivo. author: - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Veronika full_name: Bierbaum, Veronika id: 3FD04378-F248-11E8-B48F-1D18A9856A87 last_name: Bierbaum - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Teresa full_name: Tarrant, Teresa last_name: Tarrant - first_name: Tobias full_name: Bollenbach, Tobias id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87 last_name: Bollenbach orcid: 0000-0003-4398-476X - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Schwarz J, Bierbaum V, Vaahtomeri K, et al. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. 2017;27(9):1314-1325. doi:10.1016/j.cub.2017.04.004 apa: Schwarz, J., Bierbaum, V., Vaahtomeri, K., Hauschild, R., Brown, M., de Vries, I., … Sixt, M. K. (2017). Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2017.04.004 chicago: Schwarz, Jan, Veronika Bierbaum, Kari Vaahtomeri, Robert Hauschild, Markus Brown, Ingrid de Vries, Alexander F Leithner, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2017.04.004. ieee: J. Schwarz et al., “Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6,” Current Biology, vol. 27, no. 9. Cell Press, pp. 1314–1325, 2017. ista: Schwarz J, Bierbaum V, Vaahtomeri K, Hauschild R, Brown M, de Vries I, Leithner AF, Reversat A, Merrin J, Tarrant T, Bollenbach MT, Sixt MK. 2017. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. 27(9), 1314–1325. mla: Schwarz, Jan, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current Biology, vol. 27, no. 9, Cell Press, 2017, pp. 1314–25, doi:10.1016/j.cub.2017.04.004. short: J. Schwarz, V. Bierbaum, K. Vaahtomeri, R. Hauschild, M. Brown, I. de Vries, A.F. Leithner, A. Reversat, J. Merrin, T. Tarrant, M.T. Bollenbach, M.K. Sixt, Current Biology 27 (2017) 1314–1325. date_created: 2018-12-11T11:47:51Z date_published: 2017-05-09T00:00:00Z date_updated: 2023-02-23T12:50:44Z day: '09' department: - _id: MiSi - _id: Bio - _id: NanoFab doi: 10.1016/j.cub.2017.04.004 ec_funded: 1 intvolume: ' 27' issue: '9' language: - iso: eng month: '05' oa_version: None page: 1314 - 1325 project: - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Current Biology publication_identifier: issn: - '09609822' publication_status: published publisher: Cell Press publist_id: '7050' quality_controlled: '1' scopus_import: 1 status: public title: Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6 type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 27 year: '2017' ... --- _id: '677' abstract: - lang: eng text: The INO80 complex (INO80-C) is an evolutionarily conserved nucleosome remodeler that acts in transcription, replication, and genome stability. It is required for resistance against genotoxic agents and is involved in the repair of DNA double-strand breaks (DSBs) by homologous recombination (HR). However, the causes of the HR defect in INO80-C mutant cells are controversial. Here, we unite previous findings using a system to study HR with high spatial resolution in budding yeast. We find that INO80-C has at least two distinct functions during HR—DNA end resection and presynaptic filament formation. Importantly, the second function is linked to the histone variant H2A.Z. In the absence of H2A.Z, presynaptic filament formation and HR are restored in INO80-C-deficient mutants, suggesting that presynaptic filament formation is the crucial INO80-C function during HR. author: - first_name: Claudio full_name: Lademann, Claudio last_name: Lademann - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Boris full_name: Pfander, Boris last_name: Pfander - first_name: Stefan full_name: Jentsch, Stefan last_name: Jentsch citation: ama: Lademann C, Renkawitz J, Pfander B, Jentsch S. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. 2017;19(7):1294-1303. doi:10.1016/j.celrep.2017.04.051 apa: Lademann, C., Renkawitz, J., Pfander, B., & Jentsch, S. (2017). The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.051 chicago: Lademann, Claudio, Jörg Renkawitz, Boris Pfander, and Stefan Jentsch. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.051. ieee: C. Lademann, J. Renkawitz, B. Pfander, and S. Jentsch, “The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination,” Cell Reports, vol. 19, no. 7. Cell Press, pp. 1294–1303, 2017. ista: Lademann C, Renkawitz J, Pfander B, Jentsch S. 2017. The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination. Cell Reports. 19(7), 1294–1303. mla: Lademann, Claudio, et al. “The INO80 Complex Removes H2A.Z to Promote Presynaptic Filament Formation during Homologous Recombination.” Cell Reports, vol. 19, no. 7, Cell Press, 2017, pp. 1294–303, doi:10.1016/j.celrep.2017.04.051. short: C. Lademann, J. Renkawitz, B. Pfander, S. Jentsch, Cell Reports 19 (2017) 1294–1303. date_created: 2018-12-11T11:47:52Z date_published: 2017-05-16T00:00:00Z date_updated: 2021-01-12T08:08:57Z day: '16' ddc: - '570' department: - _id: MiSi doi: 10.1016/j.celrep.2017.04.051 file: - access_level: open_access checksum: efc7287d9c6354983cb151880e9ad72a content_type: application/pdf creator: system date_created: 2018-12-12T10:15:48Z date_updated: 2020-07-14T12:47:40Z file_id: '5171' file_name: IST-2017-899-v1+1_1-s2.0-S2211124717305454-main.pdf file_size: 3005610 relation: main_file file_date_updated: 2020-07-14T12:47:40Z has_accepted_license: '1' intvolume: ' 19' issue: '7' language: - iso: eng month: '05' oa: 1 oa_version: Published Version page: 1294 - 1303 publication: Cell Reports publication_identifier: issn: - '22111247' publication_status: published publisher: Cell Press publist_id: '7046' pubrep_id: '899' quality_controlled: '1' scopus_import: 1 status: public title: The INO80 complex removes H2A.Z to promote presynaptic filament formation during homologous recombination tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 19 year: '2017' ... --- _id: '694' abstract: - lang: eng text: A change regarding the extent of adhesion - hereafter referred to as adhesion plasticity - between adhesive and less-adhesive states of mammalian cells is important for their behavior. To investigate adhesion plasticity, we have selected a stable isogenic subpopulation of human MDA-MB-468 breast carcinoma cells growing in suspension. These suspension cells are unable to re-adhere to various matrices or to contract three-dimensional collagen lattices. By using transcriptome analysis, we identified the focal adhesion protein tensin3 (Tns3) as a determinant of adhesion plasticity. Tns3 is strongly reduced at mRNA and protein levels in suspension cells. Furthermore, by transiently challenging breast cancer cells to grow under non-adherent conditions markedly reduces Tns3 protein expression, which is regained upon re-adhesion. Stable knockdown of Tns3 in parental MDA-MB-468 cells results in defective adhesion, spreading and migration. Tns3-knockdown cells display impaired structure and dynamics of focal adhesion complexes as determined by immunostaining. Restoration of Tns3 protein expression in suspension cells partially rescues adhesion and focal contact composition. Our work identifies Tns3 as a crucial focal adhesion component regulated by, and functionally contributing to, the switch between adhesive and non-adhesive states in MDA-MB-468 cancer cells. article_type: original author: - first_name: Astrid full_name: Veß, Astrid last_name: Veß - first_name: Ulrich full_name: Blache, Ulrich last_name: Blache - first_name: Laura full_name: Leitner, Laura last_name: Leitner - first_name: Angela full_name: Kurz, Angela last_name: Kurz - first_name: Anja full_name: Ehrenpfordt, Anja last_name: Ehrenpfordt - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Guido full_name: Posern, Guido last_name: Posern citation: ama: Veß A, Blache U, Leitner L, et al. A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. 2017;130(13):2172-2184. doi:10.1242/jcs.200899 apa: Veß, A., Blache, U., Leitner, L., Kurz, A., Ehrenpfordt, A., Sixt, M. K., & Posern, G. (2017). A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.200899 chicago: Veß, Astrid, Ulrich Blache, Laura Leitner, Angela Kurz, Anja Ehrenpfordt, Michael K Sixt, and Guido Posern. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell Science. Company of Biologists, 2017. https://doi.org/10.1242/jcs.200899. ieee: A. Veß et al., “A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity,” Journal of Cell Science, vol. 130, no. 13. Company of Biologists, pp. 2172–2184, 2017. ista: Veß A, Blache U, Leitner L, Kurz A, Ehrenpfordt A, Sixt MK, Posern G. 2017. A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. 130(13), 2172–2184. mla: Veß, Astrid, et al. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell Science, vol. 130, no. 13, Company of Biologists, 2017, pp. 2172–84, doi:10.1242/jcs.200899. short: A. Veß, U. Blache, L. Leitner, A. Kurz, A. Ehrenpfordt, M.K. Sixt, G. Posern, Journal of Cell Science 130 (2017) 2172–2184. date_created: 2018-12-11T11:47:58Z date_published: 2017-07-01T00:00:00Z date_updated: 2021-01-12T08:09:41Z day: '01' ddc: - '570' department: - _id: MiSi doi: 10.1242/jcs.200899 external_id: pmid: - '28515231' file: - access_level: open_access checksum: 42c81a0a4fc3128883b391c3af3f74bc content_type: application/pdf creator: dernst date_created: 2019-10-24T09:43:56Z date_updated: 2020-07-14T12:47:45Z file_id: '6966' file_name: 2017_CellScience_Vess.pdf file_size: 10847596 relation: main_file file_date_updated: 2020-07-14T12:47:45Z has_accepted_license: '1' intvolume: ' 130' issue: '13' language: - iso: eng month: '07' oa: 1 oa_version: Published Version page: 2172 - 2184 pmid: 1 publication: Journal of Cell Science publication_identifier: issn: - '00219533' publication_status: published publisher: Company of Biologists publist_id: '7008' quality_controlled: '1' scopus_import: 1 status: public title: A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 130 year: '2017' ... --- _id: '1161' abstract: - lang: eng text: Coordinated changes of cell shape are often the result of the excitable, wave-like dynamics of the actin cytoskeleton. New work shows that, in migrating cells, protrusion waves arise from mechanochemical crosstalk between adhesion sites, membrane tension and the actin protrusive machinery. article_processing_charge: No author: - first_name: Jan full_name: Müller, Jan id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D last_name: Müller - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Müller J, Sixt MK. Cell migration: Making the waves. Current Biology. 2017;27(1):R24-R25. doi:10.1016/j.cub.2016.11.035' apa: 'Müller, J., & Sixt, M. K. (2017). Cell migration: Making the waves. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2016.11.035' chicago: 'Müller, Jan, and Michael K Sixt. “Cell Migration: Making the Waves.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2016.11.035.' ieee: 'J. Müller and M. K. Sixt, “Cell migration: Making the waves,” Current Biology, vol. 27, no. 1. Cell Press, pp. R24–R25, 2017.' ista: 'Müller J, Sixt MK. 2017. Cell migration: Making the waves. Current Biology. 27(1), R24–R25.' mla: 'Müller, Jan, and Michael K. Sixt. “Cell Migration: Making the Waves.” Current Biology, vol. 27, no. 1, Cell Press, 2017, pp. R24–25, doi:10.1016/j.cub.2016.11.035.' short: J. Müller, M.K. Sixt, Current Biology 27 (2017) R24–R25. date_created: 2018-12-11T11:50:29Z date_published: 2017-01-09T00:00:00Z date_updated: 2023-09-20T11:28:19Z day: '09' department: - _id: MiSi doi: 10.1016/j.cub.2016.11.035 external_id: isi: - '000391902500010' intvolume: ' 27' isi: 1 issue: '1' language: - iso: eng month: '01' oa_version: None page: R24 - R25 publication: Current Biology publication_identifier: issn: - '09609822' publication_status: published publisher: Cell Press publist_id: '6197' quality_controlled: '1' scopus_import: '1' status: public title: 'Cell migration: Making the waves' type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 27 year: '2017' ... --- _id: '727' abstract: - lang: eng text: 'Actin filaments polymerizing against membranes power endocytosis, vesicular traffic, and cell motility. In vitro reconstitution studies suggest that the structure and the dynamics of actin networks respond to mechanical forces. We demonstrate that lamellipodial actin of migrating cells responds to mechanical load when membrane tension is modulated. In a steady state, migrating cell filaments assume the canonical dendritic geometry, defined by Arp2/3-generated 70° branch points. Increased tension triggers a dense network with a broadened range of angles, whereas decreased tension causes a shift to a sparse configuration dominated by filaments growing perpendicularly to the plasma membrane. We show that these responses emerge from the geometry of branched actin: when load per filament decreases, elongation speed increases and perpendicular filaments gradually outcompete others because they polymerize the shortest distance to the membrane, where they are protected from capping. This network-intrinsic geometrical adaptation mechanism tunes protrusive force in response to mechanical load.' acknowledged_ssus: - _id: ScienComp article_processing_charge: No author: - first_name: Jan full_name: Mueller, Jan last_name: Mueller - first_name: Gregory full_name: Szep, Gregory id: 4BFB7762-F248-11E8-B48F-1D18A9856A87 last_name: Szep - first_name: Maria full_name: Nemethova, Maria id: 34E27F1C-F248-11E8-B48F-1D18A9856A87 last_name: Nemethova - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Arnon full_name: Lieber, Arnon last_name: Lieber - first_name: Christoph full_name: Winkler, Christoph last_name: Winkler - first_name: Karsten full_name: Kruse, Karsten last_name: Kruse - first_name: John full_name: Small, John last_name: Small - first_name: Christian full_name: Schmeiser, Christian last_name: Schmeiser - first_name: Kinneret full_name: Keren, Kinneret last_name: Keren - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Mueller J, Szep G, Nemethova M, et al. Load adaptation of lamellipodial actin networks. Cell. 2017;171(1):188-200. doi:10.1016/j.cell.2017.07.051 apa: Mueller, J., Szep, G., Nemethova, M., de Vries, I., Lieber, A., Winkler, C., … Sixt, M. K. (2017). Load adaptation of lamellipodial actin networks. Cell. Cell Press. https://doi.org/10.1016/j.cell.2017.07.051 chicago: Mueller, Jan, Gregory Szep, Maria Nemethova, Ingrid de Vries, Arnon Lieber, Christoph Winkler, Karsten Kruse, et al. “Load Adaptation of Lamellipodial Actin Networks.” Cell. Cell Press, 2017. https://doi.org/10.1016/j.cell.2017.07.051. ieee: J. Mueller et al., “Load adaptation of lamellipodial actin networks,” Cell, vol. 171, no. 1. Cell Press, pp. 188–200, 2017. ista: Mueller J, Szep G, Nemethova M, de Vries I, Lieber A, Winkler C, Kruse K, Small J, Schmeiser C, Keren K, Hauschild R, Sixt MK. 2017. Load adaptation of lamellipodial actin networks. Cell. 171(1), 188–200. mla: Mueller, Jan, et al. “Load Adaptation of Lamellipodial Actin Networks.” Cell, vol. 171, no. 1, Cell Press, 2017, pp. 188–200, doi:10.1016/j.cell.2017.07.051. short: J. Mueller, G. Szep, M. Nemethova, I. de Vries, A. Lieber, C. Winkler, K. Kruse, J. Small, C. Schmeiser, K. Keren, R. Hauschild, M.K. Sixt, Cell 171 (2017) 188–200. date_created: 2018-12-11T11:48:10Z date_published: 2017-09-21T00:00:00Z date_updated: 2023-09-28T11:33:49Z day: '21' department: - _id: MiSi - _id: Bio doi: 10.1016/j.cell.2017.07.051 ec_funded: 1 external_id: isi: - '000411331800020' intvolume: ' 171' isi: 1 issue: '1' language: - iso: eng month: '09' oa_version: None page: 188 - 200 project: - _id: 25AD6156-B435-11E9-9278-68D0E5697425 grant_number: LS13-029 name: Modeling of Polarization and Motility of Leukocytes in Three-Dimensional Environments - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Cell publication_identifier: issn: - '00928674' publication_status: published publisher: Cell Press publist_id: '6951' quality_controlled: '1' scopus_import: '1' status: public title: Load adaptation of lamellipodial actin networks type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 171 year: '2017' ... --- _id: '5567' abstract: - lang: eng text: Immunological synapse DC-Tcells article_processing_charge: No author: - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X citation: ama: Leithner AF. Immunological synapse DC-Tcells. 2017. doi:10.15479/AT:ISTA:71 apa: Leithner, A. F. (2017). Immunological synapse DC-Tcells. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:71 chicago: Leithner, Alexander F. “Immunological Synapse DC-Tcells.” Institute of Science and Technology Austria, 2017. https://doi.org/10.15479/AT:ISTA:71. ieee: A. F. Leithner, “Immunological synapse DC-Tcells.” Institute of Science and Technology Austria, 2017. ista: Leithner AF. 2017. Immunological synapse DC-Tcells, Institute of Science and Technology Austria, 10.15479/AT:ISTA:71. mla: Leithner, Alexander F. Immunological Synapse DC-Tcells. Institute of Science and Technology Austria, 2017, doi:10.15479/AT:ISTA:71. short: A.F. Leithner, (2017). datarep_id: '71' date_created: 2018-12-12T12:31:34Z date_published: 2017-08-09T00:00:00Z date_updated: 2024-02-21T13:47:00Z day: '09' ddc: - '570' department: - _id: MiSi doi: 10.15479/AT:ISTA:71 file: - access_level: open_access checksum: 3d6942d47d0737d064706b5728c4d8c8 content_type: video/x-msvideo creator: system date_created: 2018-12-12T13:02:47Z date_updated: 2020-07-14T12:47:04Z file_id: '5612' file_name: IST-2017-71-v1+1_Synapse_1.avi file_size: 236204020 relation: main_file - access_level: open_access checksum: 4850006c047b0147a9e85b3c2f6f0af4 content_type: video/x-msvideo creator: system date_created: 2018-12-12T13:02:51Z date_updated: 2020-07-14T12:47:04Z file_id: '5613' file_name: IST-2017-71-v1+2_Synapse_2.avi file_size: 226232496 relation: main_file file_date_updated: 2020-07-14T12:47:04Z has_accepted_license: '1' keyword: - Immunological synapse license: https://creativecommons.org/publicdomain/zero/1.0/ month: '08' oa: 1 oa_version: Published Version publisher: Institute of Science and Technology Austria status: public title: Immunological synapse DC-Tcells tmp: image: /images/cc_0.png legal_code_url: https://creativecommons.org/publicdomain/zero/1.0/legalcode name: Creative Commons Public Domain Dedication (CC0 1.0) short: CC0 (1.0) type: research_data user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2017' ... --- _id: '664' abstract: - lang: eng text: Immune cells communicate using cytokine signals, but the quantitative rules of this communication aren't clear. In this issue of Immunity, Oyler-Yaniv et al. (2017) suggest that the distribution of a cytokine within a lymphatic organ is primarily governed by the local density of cells consuming it. author: - first_name: Frank P full_name: Assen, Frank P id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87 last_name: Assen orcid: 0000-0003-3470-6119 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Assen FP, Sixt MK. The dynamic cytokine niche. Immunity. 2017;46(4):519-520. doi:10.1016/j.immuni.2017.04.006 apa: Assen, F. P., & Sixt, M. K. (2017). The dynamic cytokine niche. Immunity. Cell Press. https://doi.org/10.1016/j.immuni.2017.04.006 chicago: Assen, Frank P, and Michael K Sixt. “The Dynamic Cytokine Niche.” Immunity. Cell Press, 2017. https://doi.org/10.1016/j.immuni.2017.04.006. ieee: F. P. Assen and M. K. Sixt, “The dynamic cytokine niche,” Immunity, vol. 46, no. 4. Cell Press, pp. 519–520, 2017. ista: Assen FP, Sixt MK. 2017. The dynamic cytokine niche. Immunity. 46(4), 519–520. mla: Assen, Frank P., and Michael K. Sixt. “The Dynamic Cytokine Niche.” Immunity, vol. 46, no. 4, Cell Press, 2017, pp. 519–20, doi:10.1016/j.immuni.2017.04.006. short: F.P. Assen, M.K. Sixt, Immunity 46 (2017) 519–520. date_created: 2018-12-11T11:47:47Z date_published: 2017-04-18T00:00:00Z date_updated: 2024-03-27T23:30:09Z day: '18' department: - _id: MiSi doi: 10.1016/j.immuni.2017.04.006 intvolume: ' 46' issue: '4' language: - iso: eng month: '04' oa_version: None page: 519 - 520 publication: Immunity publication_identifier: issn: - '10747613' publication_status: published publisher: Cell Press publist_id: '7065' quality_controlled: '1' related_material: record: - id: '6947' relation: dissertation_contains status: public scopus_import: 1 status: public title: The dynamic cytokine niche type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 46 year: '2017' ... --- _id: '679' abstract: - lang: eng text: Protective responses against pathogens require a rapid mobilization of resting neutrophils and the timely removal of activated ones. Neutrophils are exceptionally short-lived leukocytes, yet it remains unclear whether the lifespan of pathogen-engaged neutrophils is regulated differently from that in the circulating steady-state pool. Here, we have found that under homeostatic conditions, the mRNA-destabilizing protein tristetraprolin (TTP) regulates apoptosis and the numbers of activated infiltrating murine neutrophils but not neutrophil cellularity. Activated TTP-deficient neutrophils exhibited decreased apoptosis and enhanced accumulation at the infection site. In the context of myeloid-specific deletion of Ttp, the potentiation of neutrophil deployment protected mice against lethal soft tissue infection with Streptococcus pyogenes and prevented bacterial dissemination. Neutrophil transcriptome analysis revealed that decreased apoptosis of TTP-deficient neutrophils was specifically associated with elevated expression of myeloid cell leukemia 1 (Mcl1) but not other antiapoptotic B cell leukemia/ lymphoma 2 (Bcl2) family members. Higher Mcl1 expression resulted from stabilization of Mcl1 mRNA in the absence of TTP. The low apoptosis rate of infiltrating TTP-deficient neutrophils was comparable to that of transgenic Mcl1-overexpressing neutrophils. Our study demonstrates that posttranscriptional gene regulation by TTP schedules the termination of the antimicrobial engagement of neutrophils. The balancing role of TTP comes at the cost of an increased risk of bacterial infections. acknowledgement: This work was supported by grants from the Austrian Science Fund (FWF) (P27538-B21, I1621-B22, and SFB 43, to PK); by funding from the European Union Seventh Framework Programme Marie Curie Initial Training Networks (FP7-PEOPLE-2012-ITN) for the project INBIONET (INfection BIOlogy Training NETwork under grant agreement PITN-GA-2012-316682; and by a joint research cluster initiative of the University of Vienna and the Medical University of Vienna. author: - first_name: Florian full_name: Ebner, Florian last_name: Ebner - first_name: Vitaly full_name: Sedlyarov, Vitaly last_name: Sedlyarov - first_name: Saren full_name: Tasciyan, Saren id: 4323B49C-F248-11E8-B48F-1D18A9856A87 last_name: Tasciyan orcid: 0000-0003-1671-393X - first_name: Masa full_name: Ivin, Masa last_name: Ivin - first_name: Franz full_name: Kratochvill, Franz last_name: Kratochvill - first_name: Nina full_name: Gratz, Nina last_name: Gratz - first_name: Lukas full_name: Kenner, Lukas last_name: Kenner - first_name: Andreas full_name: Villunger, Andreas last_name: Villunger - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Pavel full_name: Kovarik, Pavel last_name: Kovarik citation: ama: Ebner F, Sedlyarov V, Tasciyan S, et al. The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. 2017;127(6):2051-2065. doi:10.1172/JCI80631 apa: Ebner, F., Sedlyarov, V., Tasciyan, S., Ivin, M., Kratochvill, F., Gratz, N., … Kovarik, P. (2017). The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. American Society for Clinical Investigation. https://doi.org/10.1172/JCI80631 chicago: Ebner, Florian, Vitaly Sedlyarov, Saren Tasciyan, Masa Ivin, Franz Kratochvill, Nina Gratz, Lukas Kenner, Andreas Villunger, Michael K Sixt, and Pavel Kovarik. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged Neutrophils during Bacterial Infection.” The Journal of Clinical Investigation. American Society for Clinical Investigation, 2017. https://doi.org/10.1172/JCI80631. ieee: F. Ebner et al., “The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection,” The Journal of Clinical Investigation, vol. 127, no. 6. American Society for Clinical Investigation, pp. 2051–2065, 2017. ista: Ebner F, Sedlyarov V, Tasciyan S, Ivin M, Kratochvill F, Gratz N, Kenner L, Villunger A, Sixt MK, Kovarik P. 2017. The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. 127(6), 2051–2065. mla: Ebner, Florian, et al. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged Neutrophils during Bacterial Infection.” The Journal of Clinical Investigation, vol. 127, no. 6, American Society for Clinical Investigation, 2017, pp. 2051–65, doi:10.1172/JCI80631. short: F. Ebner, V. Sedlyarov, S. Tasciyan, M. Ivin, F. Kratochvill, N. Gratz, L. Kenner, A. Villunger, M.K. Sixt, P. Kovarik, The Journal of Clinical Investigation 127 (2017) 2051–2065. date_created: 2018-12-11T11:47:53Z date_published: 2017-06-01T00:00:00Z date_updated: 2024-03-27T23:30:23Z day: '01' department: - _id: MiSi doi: 10.1172/JCI80631 external_id: pmid: - '28504646' intvolume: ' 127' issue: '6' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5451238/ month: '06' oa: 1 oa_version: Submitted Version page: 2051 - 2065 pmid: 1 project: - _id: 25985A36-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T00817-B21 name: The biochemical basis of PAR polarization - _id: 25E9AF9E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P27201-B22 name: Revealing the mechanisms underlying drug interactions publication: The Journal of Clinical Investigation publication_identifier: issn: - '00219738' publication_status: published publisher: American Society for Clinical Investigation publist_id: '7038' quality_controlled: '1' related_material: record: - id: '12401' relation: dissertation_contains status: public scopus_import: 1 status: public title: The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 127 year: '2017' ... --- _id: '1137' abstract: - lang: eng text: RASGRP1 is an important guanine nucleotide exchange factor and activator of the RAS-MAPK pathway following T cell antigen receptor (TCR) signaling. The consequences of RASGRP1 mutations in humans are unknown. In a patient with recurrent bacterial and viral infections, born to healthy consanguineous parents, we used homozygosity mapping and exome sequencing to identify a biallelic stop-gain variant in RASGRP1. This variant segregated perfectly with the disease and has not been reported in genetic databases. RASGRP1 deficiency was associated in T cells and B cells with decreased phosphorylation of the extracellular-signal-regulated serine kinase ERK, which was restored following expression of wild-type RASGRP1. RASGRP1 deficiency also resulted in defective proliferation, activation and motility of T cells and B cells. RASGRP1-deficient natural killer (NK) cells exhibited impaired cytotoxicity with defective granule convergence and actin accumulation. Interaction proteomics identified the dynein light chain DYNLL1 as interacting with RASGRP1, which links RASGRP1 to cytoskeletal dynamics. RASGRP1-deficient cells showed decreased activation of the GTPase RhoA. Treatment with lenalidomide increased RhoA activity and reversed the migration and activation defects of RASGRP1-deficient lymphocytes. article_processing_charge: No article_type: original author: - first_name: Elisabeth full_name: Salzer, Elisabeth last_name: Salzer - first_name: Deniz full_name: Çaǧdaş, Deniz last_name: Çaǧdaş - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Emily full_name: Mace, Emily last_name: Mace - first_name: Wojciech full_name: Garncarz, Wojciech last_name: Garncarz - first_name: Oezlem full_name: Petronczki, Oezlem last_name: Petronczki - first_name: René full_name: Platzer, René last_name: Platzer - first_name: Laurène full_name: Pfajfer, Laurène last_name: Pfajfer - first_name: Ivan full_name: Bilic, Ivan last_name: Bilic - first_name: Sol full_name: Ban, Sol last_name: Ban - first_name: Katharina full_name: Willmann, Katharina last_name: Willmann - first_name: Malini full_name: Mukherjee, Malini last_name: Mukherjee - first_name: Verena full_name: Supper, Verena last_name: Supper - first_name: Hsiangting full_name: Hsu, Hsiangting last_name: Hsu - first_name: Pinaki full_name: Banerjee, Pinaki last_name: Banerjee - first_name: Papiya full_name: Sinha, Papiya last_name: Sinha - first_name: Fabienne full_name: Mcclanahan, Fabienne last_name: Mcclanahan - first_name: Gerhard full_name: Zlabinger, Gerhard last_name: Zlabinger - first_name: Winfried full_name: Pickl, Winfried last_name: Pickl - first_name: John full_name: Gribben, John last_name: Gribben - first_name: Hannes full_name: Stockinger, Hannes last_name: Stockinger - first_name: Keiryn full_name: Bennett, Keiryn last_name: Bennett - first_name: Johannes full_name: Huppa, Johannes last_name: Huppa - first_name: Loï̈C full_name: Dupré, Loï̈C last_name: Dupré - first_name: Özden full_name: Sanal, Özden last_name: Sanal - first_name: Ulrich full_name: Jäger, Ulrich last_name: Jäger - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Ilhan full_name: Tezcan, Ilhan last_name: Tezcan - first_name: Jordan full_name: Orange, Jordan last_name: Orange - first_name: Kaan full_name: Boztug, Kaan last_name: Boztug citation: ama: Salzer E, Çaǧdaş D, Hons M, et al. RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics. Nature Immunology. 2016;17(12):1352-1360. doi:10.1038/ni.3575 apa: Salzer, E., Çaǧdaş, D., Hons, M., Mace, E., Garncarz, W., Petronczki, O., … Boztug, K. (2016). RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3575 chicago: Salzer, Elisabeth, Deniz Çaǧdaş, Miroslav Hons, Emily Mace, Wojciech Garncarz, Oezlem Petronczki, René Platzer, et al. “RASGRP1 Deficiency Causes Immunodeficiency with Impaired Cytoskeletal Dynamics.” Nature Immunology. Nature Publishing Group, 2016. https://doi.org/10.1038/ni.3575. ieee: E. Salzer et al., “RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics,” Nature Immunology, vol. 17, no. 12. Nature Publishing Group, pp. 1352–1360, 2016. ista: Salzer E, Çaǧdaş D, Hons M, Mace E, Garncarz W, Petronczki O, Platzer R, Pfajfer L, Bilic I, Ban S, Willmann K, Mukherjee M, Supper V, Hsu H, Banerjee P, Sinha P, Mcclanahan F, Zlabinger G, Pickl W, Gribben J, Stockinger H, Bennett K, Huppa J, Dupré L, Sanal Ö, Jäger U, Sixt MK, Tezcan I, Orange J, Boztug K. 2016. RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics. Nature Immunology. 17(12), 1352–1360. mla: Salzer, Elisabeth, et al. “RASGRP1 Deficiency Causes Immunodeficiency with Impaired Cytoskeletal Dynamics.” Nature Immunology, vol. 17, no. 12, Nature Publishing Group, 2016, pp. 1352–60, doi:10.1038/ni.3575. short: E. Salzer, D. Çaǧdaş, M. Hons, E. Mace, W. Garncarz, O. Petronczki, R. Platzer, L. Pfajfer, I. Bilic, S. Ban, K. Willmann, M. Mukherjee, V. Supper, H. Hsu, P. Banerjee, P. Sinha, F. Mcclanahan, G. Zlabinger, W. Pickl, J. Gribben, H. Stockinger, K. Bennett, J. Huppa, L. Dupré, Ö. Sanal, U. Jäger, M.K. Sixt, I. Tezcan, J. Orange, K. Boztug, Nature Immunology 17 (2016) 1352–1360. date_created: 2018-12-11T11:50:21Z date_published: 2016-12-01T00:00:00Z date_updated: 2021-01-12T06:48:33Z day: '01' department: - _id: MiSi doi: 10.1038/ni.3575 external_id: pmid: - '27776107' intvolume: ' 17' issue: '12' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6400263 month: '12' oa: 1 oa_version: Submitted Version page: 1352 - 1360 pmid: 1 publication: Nature Immunology publication_status: published publisher: Nature Publishing Group publist_id: '6221' quality_controlled: '1' scopus_import: 1 status: public title: RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 17 year: '2016' ... --- _id: '1142' abstract: - lang: eng text: Hemolysis drives susceptibility to bacterial infections and predicts poor outcome from sepsis. These detrimental effects are commonly considered to be a consequence of heme-iron serving as a nutrient for bacteria. We employed a Gram-negative sepsis model and found that elevated heme levels impaired the control of bacterial proliferation independently of heme-iron acquisition by pathogens. Heme strongly inhibited phagocytosis and the migration of human and mouse phagocytes by disrupting actin cytoskeletal dynamics via activation of the GTP-binding Rho family protein Cdc42 by the guanine nucleotide exchange factor DOCK8. A chemical screening approach revealed that quinine effectively prevented heme effects on the cytoskeleton, restored phagocytosis and improved survival in sepsis. These mechanistic insights provide potential therapeutic targets for patients with sepsis or hemolytic disorders. acknowledgement: 'Y. Fukui (Medical Institute of Bioregulation, Kyushu University) and J. Stein (Theodor Kocher Institute, University of Bern) are acknowledged for providing the DOCK8 deficient bone marrow. and H. Häcker (St. Judes Children''s Research Hospital) for providing the ERHBD-HoxB8-encoding retroviral construct. pSpCas9(BB)-2a-Puro (PX459) was a gift from F. Zhang (Massachusetts Institute of Technology) (Addgene plasmid # 48139) and pGRG36 was a gift from N. Craig (Johns Hopkins University School of Medicine) (Addgene plasmid # 16666). LifeAct-GFP-encoding retrovirus was kindly provided by A. Leithner (Institute of Science and Technology Austria). pSIM8 and TKC E. coli were gifts from D.L. Court (Center for Cancer Research, National Cancer Institute). We acknowledge M. Gröger and S. Rauscher for excellent technical support (Core imaging facility, Medical University of Vienna). We thank D.P. Barlow and L.R. Cheever for critical reading of the manuscript. This work was supported by the Austrian Academy of Sciences, the Science Fund of the Austrian National Bank (14107) and the Austrian Science Fund FWF (I1620-B22) in the Infect-ERA framework (to S.Knapp).' author: - first_name: Rui full_name: Martins, Rui last_name: Martins - first_name: Julia full_name: Maier, Julia last_name: Maier - first_name: Anna full_name: Gorki, Anna last_name: Gorki - first_name: Kilian full_name: Huber, Kilian last_name: Huber - first_name: Omar full_name: Sharif, Omar last_name: Sharif - first_name: Philipp full_name: Starkl, Philipp last_name: Starkl - first_name: Simona full_name: Saluzzo, Simona last_name: Saluzzo - first_name: Federica full_name: Quattrone, Federica last_name: Quattrone - first_name: Riem full_name: Gawish, Riem last_name: Gawish - first_name: Karin full_name: Lakovits, Karin last_name: Lakovits - first_name: Michael full_name: Aichinger, Michael last_name: Aichinger - first_name: Branka full_name: Radic Sarikas, Branka last_name: Radic Sarikas - first_name: Charles full_name: Lardeau, Charles last_name: Lardeau - first_name: Anastasiya full_name: Hladik, Anastasiya last_name: Hladik - first_name: Ana full_name: Korosec, Ana last_name: Korosec - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Michelle full_name: Duggan, Michelle id: 2EDEA62C-F248-11E8-B48F-1D18A9856A87 last_name: Duggan - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki - first_name: Harald full_name: Esterbauer, Harald last_name: Esterbauer - first_name: Jacques full_name: Colinge, Jacques last_name: Colinge - first_name: Stephanie full_name: Eisenbarth, Stephanie last_name: Eisenbarth - first_name: Thomas full_name: Decker, Thomas last_name: Decker - first_name: Keiryn full_name: Bennett, Keiryn last_name: Bennett - first_name: Stefan full_name: Kubicek, Stefan last_name: Kubicek - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Giulio full_name: Superti Furga, Giulio last_name: Superti Furga - first_name: Sylvia full_name: Knapp, Sylvia last_name: Knapp citation: ama: Martins R, Maier J, Gorki A, et al. Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nature Immunology. 2016;17(12):1361-1372. doi:10.1038/ni.3590 apa: Martins, R., Maier, J., Gorki, A., Huber, K., Sharif, O., Starkl, P., … Knapp, S. (2016). Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3590 chicago: Martins, Rui, Julia Maier, Anna Gorki, Kilian Huber, Omar Sharif, Philipp Starkl, Simona Saluzzo, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection via Disruption of Phagocyte Functions.” Nature Immunology. Nature Publishing Group, 2016. https://doi.org/10.1038/ni.3590. ieee: R. Martins et al., “Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions,” Nature Immunology, vol. 17, no. 12. Nature Publishing Group, pp. 1361–1372, 2016. ista: Martins R, Maier J, Gorki A, Huber K, Sharif O, Starkl P, Saluzzo S, Quattrone F, Gawish R, Lakovits K, Aichinger M, Radic Sarikas B, Lardeau C, Hladik A, Korosec A, Brown M, Vaahtomeri K, Duggan M, Kerjaschki D, Esterbauer H, Colinge J, Eisenbarth S, Decker T, Bennett K, Kubicek S, Sixt MK, Superti Furga G, Knapp S. 2016. Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nature Immunology. 17(12), 1361–1372. mla: Martins, Rui, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection via Disruption of Phagocyte Functions.” Nature Immunology, vol. 17, no. 12, Nature Publishing Group, 2016, pp. 1361–72, doi:10.1038/ni.3590. short: R. Martins, J. Maier, A. Gorki, K. Huber, O. Sharif, P. Starkl, S. Saluzzo, F. Quattrone, R. Gawish, K. Lakovits, M. Aichinger, B. Radic Sarikas, C. Lardeau, A. Hladik, A. Korosec, M. Brown, K. Vaahtomeri, M. Duggan, D. Kerjaschki, H. Esterbauer, J. Colinge, S. Eisenbarth, T. Decker, K. Bennett, S. Kubicek, M.K. Sixt, G. Superti Furga, S. Knapp, Nature Immunology 17 (2016) 1361–1372. date_created: 2018-12-11T11:50:22Z date_published: 2016-12-01T00:00:00Z date_updated: 2021-01-12T06:48:36Z day: '01' department: - _id: MiSi - _id: PeJo doi: 10.1038/ni.3590 intvolume: ' 17' issue: '12' language: - iso: eng main_file_link: - open_access: '1' url: https://ora.ox.ac.uk/objects/uuid:f53a464e-1e5b-4f08-a7d8-b6749b852b9d month: '12' oa: 1 oa_version: Submitted Version page: 1361 - 1372 publication: Nature Immunology publication_status: published publisher: Nature Publishing Group publist_id: '6216' quality_controlled: '1' scopus_import: 1 status: public title: Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 17 year: '2016' ... --- _id: '1150' abstract: - lang: eng text: When neutrophils infiltrate a site of inflammation, they have to stop at the right place to exert their effector function. In this issue of Developmental Cell, Wang et al. (2016) show that neutrophils sense reactive oxygen species via the TRPM2 channel to arrest migration at their target site. © 2016 Elsevier Inc. author: - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Renkawitz J, Sixt MK. A Radical Break Restraining Neutrophil Migration. Developmental Cell. 2016;38(5):448-450. doi:10.1016/j.devcel.2016.08.017 apa: Renkawitz, J., & Sixt, M. K. (2016). A Radical Break Restraining Neutrophil Migration. Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2016.08.017 chicago: Renkawitz, Jörg, and Michael K Sixt. “A Radical Break Restraining Neutrophil Migration.” Developmental Cell. Cell Press, 2016. https://doi.org/10.1016/j.devcel.2016.08.017. ieee: J. Renkawitz and M. K. Sixt, “A Radical Break Restraining Neutrophil Migration,” Developmental Cell, vol. 38, no. 5. Cell Press, pp. 448–450, 2016. ista: Renkawitz J, Sixt MK. 2016. A Radical Break Restraining Neutrophil Migration. Developmental Cell. 38(5), 448–450. mla: Renkawitz, Jörg, and Michael K. Sixt. “A Radical Break Restraining Neutrophil Migration.” Developmental Cell, vol. 38, no. 5, Cell Press, 2016, pp. 448–50, doi:10.1016/j.devcel.2016.08.017. short: J. Renkawitz, M.K. Sixt, Developmental Cell 38 (2016) 448–450. date_created: 2018-12-11T11:50:25Z date_published: 2016-09-12T00:00:00Z date_updated: 2021-01-12T06:48:39Z day: '12' department: - _id: MiSi doi: 10.1016/j.devcel.2016.08.017 intvolume: ' 38' issue: '5' language: - iso: eng month: '09' oa_version: None page: 448 - 450 publication: Developmental Cell publication_status: published publisher: Cell Press publist_id: '6208' quality_controlled: '1' scopus_import: 1 status: public title: A Radical Break Restraining Neutrophil Migration type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 38 year: '2016' ... --- _id: '1154' abstract: - lang: eng text: "Cellular locomotion is a central hallmark of eukaryotic life. It is governed by cell-extrinsic molecular factors, which can either emerge in the soluble phase or as immobilized, often adhesive ligands. To encode for direction, every cue must be present as a spatial or temporal gradient. Here, we developed a microfluidic chamber that allows measurement of cell migration in combined response to surface immobilized and soluble molecular gradients. As a proof of principle we study the response of dendritic cells to their major guidance cues, chemokines. The majority of data on chemokine gradient sensing is based on in vitro studies employing soluble gradients. Despite evidence suggesting that in vivo chemokines are often immobilized to sugar residues, limited information is available how cells respond to immobilized chemokines. We tracked migration of dendritic cells towards immobilized gradients of the chemokine CCL21 and varying superimposed soluble gradients of CCL19. Differential migratory patterns illustrate the potential of our setup to quantitatively study the competitive response to both types of gradients. Beyond chemokines our approach is broadly applicable to alternative systems of chemo- and haptotaxis such as cells migrating along gradients of adhesion receptor ligands vs. any soluble cue. \r\n" acknowledgement: 'This work was supported by the Swiss National Science Foundation (Ambizione fellowship; PZ00P3-154733 to M.M.), the Swiss Multiple Sclerosis Society (research support to M.M.), a fellowship from the Boehringer Ingelheim Fonds (BIF) to J.S., the European Research Council (grant ERC GA 281556) and a START award from the Austrian Science Foundation (FWF) to M.S. #BioimagingFacility' article_number: '36440' author: - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Veronika full_name: Bierbaum, Veronika id: 3FD04378-F248-11E8-B48F-1D18A9856A87 last_name: Bierbaum - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Tino full_name: Frank, Tino last_name: Frank - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Mark Tobias full_name: Bollenbach, Mark Tobias id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87 last_name: Bollenbach orcid: 0000-0003-4398-476X - first_name: Savaş full_name: Tay, Savaş last_name: Tay - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Matthias full_name: Mehling, Matthias id: 3C23B994-F248-11E8-B48F-1D18A9856A87 last_name: Mehling orcid: 0000-0001-8599-1226 citation: ama: Schwarz J, Bierbaum V, Merrin J, et al. A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients. Scientific Reports. 2016;6. doi:10.1038/srep36440 apa: Schwarz, J., Bierbaum, V., Merrin, J., Frank, T., Hauschild, R., Bollenbach, M. T., … Mehling, M. (2016). A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients. Scientific Reports. Nature Publishing Group. https://doi.org/10.1038/srep36440 chicago: Schwarz, Jan, Veronika Bierbaum, Jack Merrin, Tino Frank, Robert Hauschild, Mark Tobias Bollenbach, Savaş Tay, Michael K Sixt, and Matthias Mehling. “A Microfluidic Device for Measuring Cell Migration towards Substrate Bound and Soluble Chemokine Gradients.” Scientific Reports. Nature Publishing Group, 2016. https://doi.org/10.1038/srep36440. ieee: J. Schwarz et al., “A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients,” Scientific Reports, vol. 6. Nature Publishing Group, 2016. ista: Schwarz J, Bierbaum V, Merrin J, Frank T, Hauschild R, Bollenbach MT, Tay S, Sixt MK, Mehling M. 2016. A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients. Scientific Reports. 6, 36440. mla: Schwarz, Jan, et al. “A Microfluidic Device for Measuring Cell Migration towards Substrate Bound and Soluble Chemokine Gradients.” Scientific Reports, vol. 6, 36440, Nature Publishing Group, 2016, doi:10.1038/srep36440. short: J. Schwarz, V. Bierbaum, J. Merrin, T. Frank, R. Hauschild, M.T. Bollenbach, S. Tay, M.K. Sixt, M. Mehling, Scientific Reports 6 (2016). date_created: 2018-12-11T11:50:27Z date_published: 2016-11-07T00:00:00Z date_updated: 2021-01-12T06:48:41Z day: '07' ddc: - '579' department: - _id: MiSi - _id: NanoFab - _id: Bio - _id: ToBo doi: 10.1038/srep36440 ec_funded: 1 file: - access_level: open_access content_type: application/pdf creator: system date_created: 2018-12-12T10:09:32Z date_updated: 2018-12-12T10:09:32Z file_id: '4756' file_name: IST-2017-744-v1+1_srep36440.pdf file_size: 2353456 relation: main_file file_date_updated: 2018-12-12T10:09:32Z has_accepted_license: '1' intvolume: ' 6' language: - iso: eng month: '11' oa: 1 oa_version: Published Version project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Scientific Reports publication_status: published publisher: Nature Publishing Group publist_id: '6204' pubrep_id: '744' quality_controlled: '1' scopus_import: 1 status: public title: A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 6 year: '2016' ... --- _id: '1201' abstract: - lang: eng text: In this issue of Cell, Skau et al. show that the formin FMN2 organizes a perinuclear actin cytoskeleton that protects the nucleus and its genomic content of migrating cells squeezing through small spaces. author: - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Renkawitz J, Sixt MK. Formin’ a nuclear protection. Cell. 2016;167(6):1448-1449. doi:10.1016/j.cell.2016.11.024 apa: Renkawitz, J., & Sixt, M. K. (2016). Formin’ a nuclear protection. Cell. Cell Press. https://doi.org/10.1016/j.cell.2016.11.024 chicago: Renkawitz, Jörg, and Michael K Sixt. “Formin’ a Nuclear Protection.” Cell. Cell Press, 2016. https://doi.org/10.1016/j.cell.2016.11.024. ieee: J. Renkawitz and M. K. Sixt, “Formin’ a nuclear protection,” Cell, vol. 167, no. 6. Cell Press, pp. 1448–1449, 2016. ista: Renkawitz J, Sixt MK. 2016. Formin’ a nuclear protection. Cell. 167(6), 1448–1449. mla: Renkawitz, Jörg, and Michael K. Sixt. “Formin’ a Nuclear Protection.” Cell, vol. 167, no. 6, Cell Press, 2016, pp. 1448–49, doi:10.1016/j.cell.2016.11.024. short: J. Renkawitz, M.K. Sixt, Cell 167 (2016) 1448–1449. date_created: 2018-12-11T11:50:41Z date_published: 2016-12-01T00:00:00Z date_updated: 2021-01-12T06:49:03Z day: '01' department: - _id: MiSi doi: 10.1016/j.cell.2016.11.024 intvolume: ' 167' issue: '6' language: - iso: eng month: '12' oa_version: None page: 1448 - 1449 publication: Cell publication_status: published publisher: Cell Press publist_id: '6149' quality_controlled: '1' scopus_import: 1 status: public title: Formin’ a nuclear protection type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 167 year: '2016' ... --- _id: '1217' abstract: - lang: eng text: Understanding the regulation of T-cell responses during inflammation and auto-immunity is fundamental for designing efficient therapeutic strategies against immune diseases. In this regard, prostaglandin E 2 (PGE 2) is mostly considered a myeloid-derived immunosuppressive molecule. We describe for the first time that T cells secrete PGE 2 during T-cell receptor stimulation. In addition, we show that autocrine PGE 2 signaling through EP receptors is essential for optimal CD4 + T-cell activation in vitro and in vivo, and for T helper 1 (Th1) and regulatory T cell differentiation. PGE 2 was found to provide additive co-stimulatory signaling through AKT activation. Intravital multiphoton microscopy showed that triggering EP receptors in T cells is also essential for the stability of T cell-dendritic cell (DC) interactions and Th-cell accumulation in draining lymph nodes (LNs) during inflammation. We further demonstrated that blocking EP receptors in T cells during the initial phase of collagen-induced arthritis in mice resulted in a reduction of clinical arthritis. This could be attributable to defective T-cell activation, accompanied by a decline in activated and interferon-γ-producing CD4 + Th1 cells in draining LNs. In conclusion, we prove that T lymphocytes secret picomolar concentrations of PGE 2, which in turn provide additive co-stimulatory signaling, enabling T cells to attain a favorable activation threshold. PGE 2 signaling in T cells is also required for maintaining long and stable interactions with DCs within LNs. Blockade of EP receptors in vivo impairs T-cell activation and development of T cell-mediated inflammatory responses. This may have implications in various pathophysiological settings. acknowledgement: This manuscript has been supported by grants SAF2007-61716 and S-SAL-0159/2006 awarded by the Spanish Ministry of Science and Education and the Community of Madrid to Dr M Fresno. author: - first_name: Vinatha full_name: Sreeramkumar, Vinatha last_name: Sreeramkumar - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Carmen full_name: Punzón, Carmen last_name: Punzón - first_name: Jens full_name: Stein, Jens last_name: Stein - first_name: David full_name: Sancho, David last_name: Sancho - first_name: Manuel full_name: Fresno Forcelledo, Manuel last_name: Fresno Forcelledo - first_name: Natalia full_name: Cuesta, Natalia last_name: Cuesta citation: ama: Sreeramkumar V, Hons M, Punzón C, et al. Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors. Immunology and Cell Biology. 2016;94(1):39-51. doi:10.1038/icb.2015.62 apa: Sreeramkumar, V., Hons, M., Punzón, C., Stein, J., Sancho, D., Fresno Forcelledo, M., & Cuesta, N. (2016). Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors. Immunology and Cell Biology. Nature Publishing Group. https://doi.org/10.1038/icb.2015.62 chicago: Sreeramkumar, Vinatha, Miroslav Hons, Carmen Punzón, Jens Stein, David Sancho, Manuel Fresno Forcelledo, and Natalia Cuesta. “Efficient T-Cell Priming and Activation Requires Signaling through Prostaglandin E2 (EP) Receptors.” Immunology and Cell Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/icb.2015.62. ieee: V. Sreeramkumar et al., “Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors,” Immunology and Cell Biology, vol. 94, no. 1. Nature Publishing Group, pp. 39–51, 2016. ista: Sreeramkumar V, Hons M, Punzón C, Stein J, Sancho D, Fresno Forcelledo M, Cuesta N. 2016. Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors. Immunology and Cell Biology. 94(1), 39–51. mla: Sreeramkumar, Vinatha, et al. “Efficient T-Cell Priming and Activation Requires Signaling through Prostaglandin E2 (EP) Receptors.” Immunology and Cell Biology, vol. 94, no. 1, Nature Publishing Group, 2016, pp. 39–51, doi:10.1038/icb.2015.62. short: V. Sreeramkumar, M. Hons, C. Punzón, J. Stein, D. Sancho, M. Fresno Forcelledo, N. Cuesta, Immunology and Cell Biology 94 (2016) 39–51. date_created: 2018-12-11T11:50:46Z date_published: 2016-01-01T00:00:00Z date_updated: 2021-01-12T06:49:09Z day: '01' department: - _id: MiSi doi: 10.1038/icb.2015.62 intvolume: ' 94' issue: '1' language: - iso: eng month: '01' oa_version: None page: 39 - 51 publication: Immunology and Cell Biology publication_status: published publisher: Nature Publishing Group publist_id: '6116' quality_controlled: '1' scopus_import: 1 status: public title: Efficient T-cell priming and activation requires signaling through prostaglandin E2 (EP) receptors type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 94 year: '2016' ... --- _id: '1285' abstract: - lang: eng text: Cell migration is central to a multitude of physiological processes, including embryonic development, immune surveillance, and wound healing, and deregulated migration is key to cancer dissemination. Decades of investigations have uncovered many of the molecular and physical mechanisms underlying cell migration. Together with protrusion extension and cell body retraction, adhesion to the substrate via specific focal adhesion points has long been considered an essential step in cell migration. Although this is true for cells moving on two-dimensional substrates, recent studies have demonstrated that focal adhesions are not required for cells moving in three dimensions, in which confinement is sufficient to maintain a cell in contact with its substrate. Here, we review the investigations that have led to challenging the requirement of specific adhesions for migration, discuss the physical mechanisms proposed for cell body translocation during focal adhesion-independent migration, and highlight the remaining open questions for the future. acknowledgement: We would like to thank Dani Bodor for critical comments on the manuscript and Guillaume Salbreux for discussions. The authors are supported by the United Kingdom's Medical Research Council (MRC) (E.K.P. and I.M.A.; core funding to the MRC Laboratory for Molecular Cell Biology), by the European Research Council [ERC GA 311637 (E.K.P.) and ERC GA 281556 (M.S.)], and by a START award from the Austrian Science Foundation (M.S.). author: - first_name: Ewa full_name: Paluch, Ewa last_name: Paluch - first_name: Irene full_name: Aspalter, Irene last_name: Aspalter - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Paluch E, Aspalter I, Sixt MK. Focal adhesion-independent cell migration. Annual Review of Cell and Developmental Biology. 2016;32:469-490. doi:10.1146/annurev-cellbio-111315-125341 apa: Paluch, E., Aspalter, I., & Sixt, M. K. (2016). Focal adhesion-independent cell migration. Annual Review of Cell and Developmental Biology. Annual Reviews. https://doi.org/10.1146/annurev-cellbio-111315-125341 chicago: Paluch, Ewa, Irene Aspalter, and Michael K Sixt. “Focal Adhesion-Independent Cell Migration.” Annual Review of Cell and Developmental Biology. Annual Reviews, 2016. https://doi.org/10.1146/annurev-cellbio-111315-125341. ieee: E. Paluch, I. Aspalter, and M. K. Sixt, “Focal adhesion-independent cell migration,” Annual Review of Cell and Developmental Biology, vol. 32. Annual Reviews, pp. 469–490, 2016. ista: Paluch E, Aspalter I, Sixt MK. 2016. Focal adhesion-independent cell migration. Annual Review of Cell and Developmental Biology. 32, 469–490. mla: Paluch, Ewa, et al. “Focal Adhesion-Independent Cell Migration.” Annual Review of Cell and Developmental Biology, vol. 32, Annual Reviews, 2016, pp. 469–90, doi:10.1146/annurev-cellbio-111315-125341. short: E. Paluch, I. Aspalter, M.K. Sixt, Annual Review of Cell and Developmental Biology 32 (2016) 469–490. date_created: 2018-12-11T11:51:08Z date_published: 2016-10-06T00:00:00Z date_updated: 2021-01-12T06:49:37Z day: '06' department: - _id: MiSi doi: 10.1146/annurev-cellbio-111315-125341 ec_funded: 1 intvolume: ' 32' language: - iso: eng month: '10' oa_version: None page: 469 - 490 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Annual Review of Cell and Developmental Biology publication_status: published publisher: Annual Reviews publist_id: '6031' quality_controlled: '1' scopus_import: 1 status: public title: Focal adhesion-independent cell migration type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 32 year: '2016' ... --- _id: '1490' abstract: - lang: eng text: To induce adaptive immunity, dendritic cells (DCs) migrate through afferent lymphatic vessels (LVs) to draining lymph nodes (dLNs). This process occurs in several consecutive steps. Upon entry into lymphatic capillaries, DCs first actively crawl into downstream collecting vessels. From there, they are next passively and rapidly transported to the dLN by lymph flow. Here, we describe a role for the chemokine CCL21 in intralymphatic DC crawling. Performing time-lapse imaging in murine skin, we found that blockade of CCL21-but not the absence of lymph flow-completely abolished DC migration from capillaries toward collecting vessels and reduced the ability of intralymphatic DCs to emigrate from skin. Moreover, we found that in vitro low laminar flow established a CCL21 gradient along lymphatic endothelial monolayers, thereby inducing downstream-directed DC migration. These findings reveal a role for intralymphatic CCL21 in promoting DC trafficking to dLNs, through the formation of a flow-induced gradient. author: - first_name: Erica full_name: Russo, Erica last_name: Russo - first_name: Alvaro full_name: Teijeira, Alvaro last_name: Teijeira - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Ann full_name: Willrodt, Ann last_name: Willrodt - first_name: Joël full_name: Bloch, Joël last_name: Bloch - first_name: Maximilian full_name: Nitschké, Maximilian last_name: Nitschké - first_name: Laura full_name: Santambrogio, Laura last_name: Santambrogio - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Cornelia full_name: Halin, Cornelia last_name: Halin citation: ama: Russo E, Teijeira A, Vaahtomeri K, et al. Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels. Cell Reports. 2016;14(7):1723-1734. doi:10.1016/j.celrep.2016.01.048 apa: Russo, E., Teijeira, A., Vaahtomeri, K., Willrodt, A., Bloch, J., Nitschké, M., … Halin, C. (2016). Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2016.01.048 chicago: Russo, Erica, Alvaro Teijeira, Kari Vaahtomeri, Ann Willrodt, Joël Bloch, Maximilian Nitschké, Laura Santambrogio, Dontscho Kerjaschki, Michael K Sixt, and Cornelia Halin. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic Cells through Afferent Lymphatic Vessels.” Cell Reports. Cell Press, 2016. https://doi.org/10.1016/j.celrep.2016.01.048. ieee: E. Russo et al., “Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels,” Cell Reports, vol. 14, no. 7. Cell Press, pp. 1723–1734, 2016. ista: Russo E, Teijeira A, Vaahtomeri K, Willrodt A, Bloch J, Nitschké M, Santambrogio L, Kerjaschki D, Sixt MK, Halin C. 2016. Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels. Cell Reports. 14(7), 1723–1734. mla: Russo, Erica, et al. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic Cells through Afferent Lymphatic Vessels.” Cell Reports, vol. 14, no. 7, Cell Press, 2016, pp. 1723–34, doi:10.1016/j.celrep.2016.01.048. short: E. Russo, A. Teijeira, K. Vaahtomeri, A. Willrodt, J. Bloch, M. Nitschké, L. Santambrogio, D. Kerjaschki, M.K. Sixt, C. Halin, Cell Reports 14 (2016) 1723–1734. date_created: 2018-12-11T11:52:19Z date_published: 2016-02-23T00:00:00Z date_updated: 2021-01-12T06:51:07Z day: '23' ddc: - '570' department: - _id: MiSi doi: 10.1016/j.celrep.2016.01.048 file: - access_level: open_access checksum: c98c1151d5f1e5ce1643a83d8d7f3c29 content_type: application/pdf creator: system date_created: 2018-12-12T10:12:30Z date_updated: 2020-07-14T12:44:58Z file_id: '4948' file_name: IST-2016-515-v1+1_1-s2.0-S2211124716300262-main.pdf file_size: 5489897 relation: main_file file_date_updated: 2020-07-14T12:44:58Z has_accepted_license: '1' intvolume: ' 14' issue: '7' language: - iso: eng month: '02' oa: 1 oa_version: Published Version page: 1723 - 1734 publication: Cell Reports publication_status: published publisher: Cell Press publist_id: '5697' pubrep_id: '515' quality_controlled: '1' scopus_import: 1 status: public title: Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 14 year: '2016' ... --- _id: '1599' abstract: - lang: eng text: "The addition of polysialic acid to N- and/or O-linked glycans, referred to as polysialylation, is a rare posttranslational modification that is mainly known to control the developmental plasticity of the nervous system. Here we show that CCR7, the central chemokine receptor controlling immune cell trafficking to secondary lymphatic organs, carries polysialic acid. This modification is essential for the recognition of the CCR7 ligand CCL21. As a consequence, dendritic cell trafficking is abrogated in polysialyltransferase-deficient mice, manifesting as disturbed lymph node homeostasis and unresponsiveness to inflammatory stimuli. Structure-function analysis of chemokine-receptor interactions reveals that CCL21 adopts an autoinhibited conformation, which is released upon interaction with polysialic acid. Thus, we describe a glycosylation-mediated immune cell trafficking disorder and its mechanistic basis.\r\n" acknowledged_ssus: - _id: SSU acknowledgement: 'We thank S. Schüchner and E. Ogris for kindly providing the antibody to GFP, M. Helmbrecht and A. Huber for providing Nrp2−/− mice, the IST Scientific Support Facilities for excellent services, and J. Renkawitz and K. Vaahtomeri for critically reading the manuscript. ' article_processing_charge: No article_type: original author: - first_name: Eva full_name: Kiermaier, Eva id: 3EB04B78-F248-11E8-B48F-1D18A9856A87 last_name: Kiermaier orcid: 0000-0001-6165-5738 - first_name: Christine full_name: Moussion, Christine id: 3356F664-F248-11E8-B48F-1D18A9856A87 last_name: Moussion - first_name: Christopher full_name: Veldkamp, Christopher last_name: Veldkamp - first_name: Rita full_name: Gerardy Schahn, Rita last_name: Gerardy Schahn - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Larry full_name: Williams, Larry last_name: Williams - first_name: Gary full_name: Chaffee, Gary last_name: Chaffee - first_name: Andrew full_name: Phillips, Andrew last_name: Phillips - first_name: Friedrich full_name: Freiberger, Friedrich last_name: Freiberger - first_name: Richard full_name: Imre, Richard last_name: Imre - first_name: Deni full_name: Taleski, Deni last_name: Taleski - first_name: Richard full_name: Payne, Richard last_name: Payne - first_name: Asolina full_name: Braun, Asolina last_name: Braun - first_name: Reinhold full_name: Förster, Reinhold last_name: Förster - first_name: Karl full_name: Mechtler, Karl last_name: Mechtler - first_name: Martina full_name: Mühlenhoff, Martina last_name: Mühlenhoff - first_name: Brian full_name: Volkman, Brian last_name: Volkman - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Kiermaier E, Moussion C, Veldkamp C, et al. Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. Science. 2016;351(6269):186-190. doi:10.1126/science.aad0512 apa: Kiermaier, E., Moussion, C., Veldkamp, C., Gerardy  Schahn, R., de Vries, I., Williams, L., … Sixt, M. K. (2016). Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.aad0512 chicago: Kiermaier, Eva, Christine Moussion, Christopher Veldkamp, Rita Gerardy  Schahn, Ingrid de Vries, Larry Williams, Gary Chaffee, et al. “Polysialylation Controls Dendritic Cell Trafficking by Regulating Chemokine Recognition.” Science. American Association for the Advancement of Science, 2016. https://doi.org/10.1126/science.aad0512. ieee: E. Kiermaier et al., “Polysialylation controls dendritic cell trafficking by regulating chemokine recognition,” Science, vol. 351, no. 6269. American Association for the Advancement of Science, pp. 186–190, 2016. ista: Kiermaier E, Moussion C, Veldkamp C, Gerardy  Schahn R, de Vries I, Williams L, Chaffee G, Phillips A, Freiberger F, Imre R, Taleski D, Payne R, Braun A, Förster R, Mechtler K, Mühlenhoff M, Volkman B, Sixt MK. 2016. Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. Science. 351(6269), 186–190. mla: Kiermaier, Eva, et al. “Polysialylation Controls Dendritic Cell Trafficking by Regulating Chemokine Recognition.” Science, vol. 351, no. 6269, American Association for the Advancement of Science, 2016, pp. 186–90, doi:10.1126/science.aad0512. short: E. Kiermaier, C. Moussion, C. Veldkamp, R. Gerardy  Schahn, I. de Vries, L. Williams, G. Chaffee, A. Phillips, F. Freiberger, R. Imre, D. Taleski, R. Payne, A. Braun, R. Förster, K. Mechtler, M. Mühlenhoff, B. Volkman, M.K. Sixt, Science 351 (2016) 186–190. date_created: 2018-12-11T11:52:57Z date_published: 2016-01-08T00:00:00Z date_updated: 2021-01-12T06:51:52Z day: '08' department: - _id: MiSi doi: 10.1126/science.aad0512 ec_funded: 1 external_id: pmid: - '26657283' intvolume: ' 351' issue: '6269' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5583642/ month: '01' oa: 1 oa_version: Submitted Version page: 186 - 190 pmid: 1 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A76F58-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '289720' name: Stromal Cell-immune Cell Interactions in Health and Disease - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Science publication_status: published publisher: American Association for the Advancement of Science publist_id: '5570' quality_controlled: '1' scopus_import: 1 status: public title: Polysialylation controls dendritic cell trafficking by regulating chemokine recognition type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 351 year: '2016' ... --- _id: '1597' abstract: - lang: eng text: Chemokines are the main guidance cues directing leukocyte migration. Opposed to early assumptions, chemokines do not necessarily act as soluble cues but are often immobilized within tissues, e.g., dendritic cell migration toward lymphatic vessels is guided by a haptotactic gradient of the chemokine CCL21. Controlled assay systems to quantitatively study haptotaxis in vitro are still missing. In this chapter, we describe an in vitro haptotaxis assay optimized for the unique properties of dendritic cells. The chemokine CCL21 is immobilized in a bioactive state, using laser-assisted protein adsorption by photobleaching. The cells follow this immobilized CCL21 gradient in a haptotaxis chamber, which provides three dimensionally confined migration conditions. acknowledged_ssus: - _id: Bio acknowledgement: This work was supported by the Boehringer Ingelheim Fonds, the European Research Council (ERC StG 281556), and a START Award of the Austrian Science Foundation (FWF). We thank Robert Hauschild, Anne Reversat, and Jack Merrin for valuable input and the Imaging Facility of IST Austria for excellent support. article_processing_charge: No article_type: original author: - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Schwarz J, Sixt MK. Quantitative analysis of dendritic cell haptotaxis. Methods in Enzymology. 2016;570:567-581. doi:10.1016/bs.mie.2015.11.004 apa: Schwarz, J., & Sixt, M. K. (2016). Quantitative analysis of dendritic cell haptotaxis. Methods in Enzymology. Elsevier. https://doi.org/10.1016/bs.mie.2015.11.004 chicago: Schwarz, Jan, and Michael K Sixt. “Quantitative Analysis of Dendritic Cell Haptotaxis.” Methods in Enzymology. Elsevier, 2016. https://doi.org/10.1016/bs.mie.2015.11.004. ieee: J. Schwarz and M. K. Sixt, “Quantitative analysis of dendritic cell haptotaxis,” Methods in Enzymology, vol. 570. Elsevier, pp. 567–581, 2016. ista: Schwarz J, Sixt MK. 2016. Quantitative analysis of dendritic cell haptotaxis. Methods in Enzymology. 570, 567–581. mla: Schwarz, Jan, and Michael K. Sixt. “Quantitative Analysis of Dendritic Cell Haptotaxis.” Methods in Enzymology, vol. 570, Elsevier, 2016, pp. 567–81, doi:10.1016/bs.mie.2015.11.004. short: J. Schwarz, M.K. Sixt, Methods in Enzymology 570 (2016) 567–581. date_created: 2018-12-11T11:52:56Z date_published: 2016-01-01T00:00:00Z date_updated: 2021-01-12T06:51:51Z day: '01' department: - _id: MiSi doi: 10.1016/bs.mie.2015.11.004 ec_funded: 1 external_id: pmid: - '26921962' intvolume: ' 570' language: - iso: eng month: '01' oa_version: None page: 567 - 581 pmid: 1 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Methods in Enzymology publication_status: published publisher: Elsevier publist_id: '5573' quality_controlled: '1' scopus_import: 1 status: public title: Quantitative analysis of dendritic cell haptotaxis type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 570 year: '2016' ... --- _id: '1129' abstract: - lang: eng text: "Directed cell migration is a hallmark feature, present in almost all multi-cellular\r\norganisms. Despite its importance, basic questions regarding force transduction\r\nor directional sensing are still heavily investigated. Directed migration of cells\r\nguided by immobilized guidance cues - haptotaxis - occurs in key-processes,\r\nsuch as embryonic development and immunity (Middleton et al., 1997; Nguyen\r\net al., 2000; Thiery, 1984; Weber et al., 2013). Immobilized guidance cues\r\ncomprise adhesive ligands, such as collagen and fibronectin (Barczyk et al.,\r\n2009), or chemokines - the main guidance cues for migratory leukocytes\r\n(Middleton et al., 1997; Weber et al., 2013). While adhesive ligands serve as\r\nattachment sites guiding cell migration (Carter, 1965), chemokines instruct\r\nhaptotactic migration by inducing adhesion to adhesive ligands and directional\r\nguidance (Rot and Andrian, 2004; Schumann et al., 2010). Quantitative analysis\r\nof the cellular response to immobilized guidance cues requires in vitro assays\r\nthat foster cell migration, offer accurate control of the immobilized cues on a\r\nsubcellular scale and in the ideal case closely reproduce in vivo conditions. The\r\nexploration of haptotactic cell migration through design and employment of such\r\nassays represents the main focus of this work.\r\nDendritic cells (DCs) are leukocytes, which after encountering danger\r\nsignals such as pathogens in peripheral organs instruct naïve T-cells and\r\nconsequently the adaptive immune response in the lymph node (Mellman and\r\nSteinman, 2001). To reach the lymph node from the periphery, DCs follow\r\nhaptotactic gradients of the chemokine CCL21 towards lymphatic vessels\r\n(Weber et al., 2013). Questions about how DCs interpret haptotactic CCL21\r\ngradients have not yet been addressed. The main reason for this is the lack of\r\nan assay that offers diverse haptotactic environments, hence allowing the study\r\nof DC migration as a response to different signals of immobilized guidance cue.\r\nIn this work, we developed an in vitro assay that enables us to\r\nquantitatively assess DC haptotaxis, by combining precisely controllable\r\nchemokine photo-patterning with physically confining migration conditions. With this tool at hand, we studied the influence of CCL21 gradient properties and\r\nconcentration on DC haptotaxis. We found that haptotactic gradient sensing\r\ndepends on the absolute CCL21 concentration in combination with the local\r\nsteepness of the gradient. Our analysis suggests that the directionality of\r\nmigrating DCs is governed by the signal-to-noise ratio of CCL21 binding to its\r\nreceptor CCR7. Moreover, the haptotactic CCL21 gradient formed in vivo\r\nprovides an optimal shape for DCs to recognize haptotactic guidance cue.\r\nBy reconstitution of the CCL21 gradient in vitro we were also able to\r\nstudy the influence of CCR7 signal termination on DC haptotaxis. To this end,\r\nwe used DCs lacking the G-protein coupled receptor kinase GRK6, which is\r\nresponsible for CCL21 induced CCR7 receptor phosphorylation and\r\ndesensitization (Zidar et al., 2009). We found that CCR7 desensitization by\r\nGRK6 is crucial for maintenance of haptotactic CCL21 gradient sensing in vitro\r\nand confirm those observations in vivo.\r\nIn the context of the organism, immobilized haptotactic guidance cues\r\noften coincide and compete with soluble chemotactic guidance cues. During\r\nwound healing, fibroblasts are exposed and influenced by adhesive cues and\r\nsoluble factors at the same time (Wu et al., 2012; Wynn, 2008). Similarly,\r\nmigrating DCs are exposed to both, soluble chemokines (CCL19 and truncated\r\nCCL21) inducing chemotactic behavior as well as the immobilized CCL21. To\r\nquantitatively assess these complex coinciding immobilized and soluble\r\nguidance cues, we implemented our chemokine photo-patterning technique in a\r\nmicrofluidic system allowing for chemotactic gradient generation. To validate\r\nthe assay, we observed DC migration in competing CCL19/CCL21\r\nenvironments.\r\nAdhesiveness guided haptotaxis has been studied intensively over the\r\nlast century. However, quantitative studies leading to conceptual models are\r\nlargely missing, again due to the lack of a precisely controllable in vitro assay. A\r\nrequirement for such an in vitro assay is that it must prevent any uncontrolled\r\ncell adhesion. This can be accomplished by stable passivation of the surface. In\r\naddition, controlled adhesion must be sustainable, quantifiable and dose\r\ndependent in order to create homogenous gradients. Therefore, we developed a novel covalent photo-patterning technique satisfying all these needs. In\r\ncombination with a sustainable poly-vinyl alcohol (PVA) surface coating we\r\nwere able to generate gradients of adhesive cue to direct cell migration. This\r\napproach allowed us to characterize the haptotactic migratory behavior of\r\nzebrafish keratocytes in vitro. Furthermore, defined patterns of adhesive cue\r\nallowed us to control for cell shape and growth on a subcellular scale." acknowledged_ssus: - _id: Bio - _id: PreCl - _id: LifeSc acknowledgement: "First, I would like to thank Michael Sixt for being a great supervisor, mentor and\r\nscientist. I highly appreciate his guidance and continued support. Furthermore, I\r\nam very grateful that he gave me the exceptional opportunity to pursue many\r\nideas of which some managed to be included in this thesis.\r\nI owe sincere thanks to the members of my PhD thesis committee, Daria\r\nSiekhaus, Daniel Legler and Harald Janovjak. Especially I would like to thank\r\nDaria for her advice and encouragement during our regular progress meetings.\r\nI also want to thank the team and fellows of the Boehringer Ingelheim Fond\r\n(BIF) PhD Fellowship for amazing and inspiring meetings and the BIF for\r\nfinancial support.\r\nImportant factors for the success of this thesis were the warm, creative\r\nand helpful atmosphere as well as the team spirit of the whole Sixt Lab.\r\nTherefore I would like to thank my current and former colleagues Frank Assen,\r\nMarkus Brown, Ingrid de Vries, Michelle Duggan, Alexander Eichner, Miroslav\r\nHons, Eva Kiermaier, Aglaja Kopf, Alexander Leithner, Christine Moussion, Jan\r\nMüller, Maria Nemethova, Jörg Renkawitz, Anne Reversat, Kari Vaahtomeri,\r\nMichele Weber and Stefan Wieser. We had an amazing time with many\r\nlegendary evenings and events. Along these lines I want to thank the in vitro\r\ncrew of the lab, Jörg, Anne and Alex, for lots of ideas and productive\r\ndiscussions. I am sure, some day we will reveal the secret of the ‘splodge’.\r\nI want to thank the members of the Heisenberg Lab for a great time and\r\nthrilling kicker matches. In this regard I especially want to thank Maurizio\r\n‘Gnocci’ Monti, Gabriel Krens, Alex Eichner, Martin Behrndt, Vanessa Barone,Philipp Schmalhorst, Michael Smutny, Daniel Capek, Anne Reversat, Eva\r\nKiermaier, Frank Assen and Jan Müller for wonderful after-lunch matches.\r\nI would not have been able to analyze the thousands of cell trajectories\r\nand probably hundreds of thousands of mouse clicks without the productive\r\ncollaboration with Veronika Bierbaum and Tobias Bollenbach. Thanks Vroni for\r\ncountless meetings, discussions and graphs and of course for proofreading and\r\nadvice for this thesis. For proofreading I also want to thank Evi, Jörg, Jack and\r\nAnne.\r\nI would like to acknowledge Matthias Mehling for a very productive\r\ncollaboration and for introducing me into the wild world of microfluidics. Jack\r\nMerrin, for countless wafers, PDMS coated coverslips and help with anything\r\nmicro-fabrication related. And Maria Nemethova for establishing the ‘click’\r\npatterning approach with me. Without her it still would be just one of the ideas…\r\nMany thanks to Ekaterina Papusheva, Robert Hauschild, Doreen Milius\r\nand Nasser Darwish from the Bioimaging Facility as well as the Preclinical and\r\nthe Life Science facilities of IST Austria for excellent technical support. At this\r\npoint I especially want to thank Robert for countless image analyses and\r\ntechnical ideas. Always interested and creative he played an essential role in all\r\nof my projects.\r\nAdditionally I want to thank Ingrid and Gabby for welcoming me warmly\r\nwhen I first started at IST, for scientific and especially mental support in all\r\nthose years, countless coffee sessions and Heurigen evenings. #BioimagingFacility #LifeScienceFacility #PreClinicalFacility" alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz citation: ama: Schwarz J. Quantitative analysis of haptotactic cell migration. 2016. apa: Schwarz, J. (2016). Quantitative analysis of haptotactic cell migration. Institute of Science and Technology Austria. chicago: Schwarz, Jan. “Quantitative Analysis of Haptotactic Cell Migration.” Institute of Science and Technology Austria, 2016. ieee: J. Schwarz, “Quantitative analysis of haptotactic cell migration,” Institute of Science and Technology Austria, 2016. ista: Schwarz J. 2016. Quantitative analysis of haptotactic cell migration. Institute of Science and Technology Austria. mla: Schwarz, Jan. Quantitative Analysis of Haptotactic Cell Migration. Institute of Science and Technology Austria, 2016. short: J. Schwarz, Quantitative Analysis of Haptotactic Cell Migration, Institute of Science and Technology Austria, 2016. date_created: 2018-12-11T11:50:18Z date_published: 2016-07-01T00:00:00Z date_updated: 2023-09-07T11:54:33Z day: '01' ddc: - '570' degree_awarded: PhD department: - _id: MiSi file: - access_level: closed checksum: e3cd6b28f9c5cccb8891855565a2dade content_type: application/pdf creator: dernst date_created: 2019-08-13T10:55:35Z date_updated: 2019-08-13T10:55:35Z file_id: '6813' file_name: Thesis_JSchwarz_final.pdf file_size: 32044069 relation: main_file - access_level: open_access checksum: c3dbe219acf87eed2f46d21d5cca00de content_type: application/pdf creator: dernst date_created: 2021-02-22T11:43:14Z date_updated: 2021-02-22T11:43:14Z file_id: '9181' file_name: 2016_Thesis_JSchwarz.pdf file_size: 8396717 relation: main_file success: 1 file_date_updated: 2021-02-22T11:43:14Z has_accepted_license: '1' language: - iso: eng month: '07' oa: 1 oa_version: Published Version page: '178' publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria publist_id: '6231' status: public supervisor: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 title: Quantitative analysis of haptotactic cell migration type: dissertation user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 year: '2016' ... --- _id: '1321' abstract: - lang: eng text: Most migrating cells extrude their front by the force of actin polymerization. Polymerization requires an initial nucleation step, which is mediated by factors establishing either parallel filaments in the case of filopodia or branched filaments that form the branched lamellipodial network. Branches are considered essential for regular cell motility and are initiated by the Arp2/3 complex, which in turn is activated by nucleation-promoting factors of the WASP and WAVE families. Here we employed rapid amoeboid crawling leukocytes and found that deletion of the WAVE complex eliminated actin branching and thus lamellipodia formation. The cells were left with parallel filaments at the leading edge, which translated, depending on the differentiation status of the cell, into a unipolar pointed cell shape or cells with multiple filopodia. Remarkably, unipolar cells migrated with increased speed and enormous directional persistence, while they were unable to turn towards chemotactic gradients. Cells with multiple filopodia retained chemotactic activity but their migration was progressively impaired with increasing geometrical complexity of the extracellular environment. These findings establish that diversified leading edge protrusions serve as explorative structures while they slow down actual locomotion. acknowledged_ssus: - _id: SSU acknowledgement: "This work was supported by the German Research Foundation (DFG) Priority Program SP 1464 to T.E.B.S. and M.S., and European Research Council (ERC GA 281556) and Human Frontiers Program grants to M.S.\r\nService Units of IST Austria for excellent technical support." article_processing_charge: No article_type: original author: - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Alexander full_name: Eichner, Alexander id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87 last_name: Eichner - first_name: Jan full_name: Müller, Jan id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D last_name: Müller - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: David full_name: De Gorter, David last_name: De Gorter - first_name: Florian full_name: Schur, Florian id: 48AD8942-F248-11E8-B48F-1D18A9856A87 last_name: Schur orcid: 0000-0003-4790-8078 - first_name: Jonathan full_name: Bayerl, Jonathan last_name: Bayerl - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Stefan full_name: Wieser, Stefan id: 355AA5A0-F248-11E8-B48F-1D18A9856A87 last_name: Wieser orcid: 0000-0002-2670-2217 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Frank full_name: Lai, Frank last_name: Lai - first_name: Markus full_name: Moser, Markus last_name: Moser - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner - first_name: Victor full_name: Small, Victor last_name: Small - first_name: Theresia full_name: Stradal, Theresia last_name: Stradal - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Leithner AF, Eichner A, Müller J, et al. Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. 2016;18:1253-1259. doi:10.1038/ncb3426 apa: Leithner, A. F., Eichner, A., Müller, J., Reversat, A., Brown, M., Schwarz, J., … Sixt, M. K. (2016). Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb3426 chicago: Leithner, Alexander F, Alexander Eichner, Jan Müller, Anne Reversat, Markus Brown, Jan Schwarz, Jack Merrin, et al. “Diversified Actin Protrusions Promote Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature Cell Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/ncb3426. ieee: A. F. Leithner et al., “Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes,” Nature Cell Biology, vol. 18. Nature Publishing Group, pp. 1253–1259, 2016. ista: Leithner AF, Eichner A, Müller J, Reversat A, Brown M, Schwarz J, Merrin J, De Gorter D, Schur FK, Bayerl J, de Vries I, Wieser S, Hauschild R, Lai F, Moser M, Kerjaschki D, Rottner K, Small V, Stradal T, Sixt MK. 2016. Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. 18, 1253–1259. mla: Leithner, Alexander F., et al. “Diversified Actin Protrusions Promote Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature Cell Biology, vol. 18, Nature Publishing Group, 2016, pp. 1253–59, doi:10.1038/ncb3426. short: A.F. Leithner, A. Eichner, J. Müller, A. Reversat, M. Brown, J. Schwarz, J. Merrin, D. De Gorter, F.K. Schur, J. Bayerl, I. de Vries, S. Wieser, R. Hauschild, F. Lai, M. Moser, D. Kerjaschki, K. Rottner, V. Small, T. Stradal, M.K. Sixt, Nature Cell Biology 18 (2016) 1253–1259. date_created: 2018-12-11T11:51:21Z date_published: 2016-10-24T00:00:00Z date_updated: 2024-03-27T23:30:16Z day: '24' ddc: - '570' department: - _id: MiSi - _id: NanoFab - _id: Bio doi: 10.1038/ncb3426 ec_funded: 1 file: - access_level: open_access checksum: e1411cb7c99a2d9089c178a6abef25e7 content_type: application/pdf creator: dernst date_created: 2020-05-14T16:33:46Z date_updated: 2020-07-14T12:44:43Z file_id: '7844' file_name: 2018_NatureCell_Leithner.pdf file_size: 4433280 relation: main_file file_date_updated: 2020-07-14T12:44:43Z has_accepted_license: '1' intvolume: ' 18' language: - iso: eng month: '10' oa: 1 oa_version: Submitted Version page: 1253 - 1259 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Nature Cell Biology publication_status: published publisher: Nature Publishing Group publist_id: '5949' quality_controlled: '1' related_material: record: - id: '323' relation: dissertation_contains status: public scopus_import: 1 status: public title: Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 18 year: '2016' ... --- _id: '1530' abstract: - lang: eng text: In growing cells, protein synthesis and cell growth are typically not synchronous, and, thus, protein concentrations vary over the cell division cycle. We have developed a theoretical description of genetic regulatory systems in bacteria that explicitly considers the cell division cycle to investigate its impact on gene expression. We calculate the cell-to-cell variations arising from cells being at different stages in the division cycle for unregulated genes and for basic regulatory mechanisms. These variations contribute to the extrinsic noise observed in single-cell experiments, and are most significant for proteins with short lifetimes. Negative autoregulation buffers against variation of protein concentration over the division cycle, but the effect is found to be relatively weak. Stronger buffering is achieved by an increased protein lifetime. Positive autoregulation can strongly amplify such variation if the parameters are set to values that lead to resonance-like behaviour. For cooperative positive autoregulation, the concentration variation over the division cycle diminishes the parameter region of bistability and modulates the switching times between the two stable states. The same effects are seen for a two-gene mutual-repression toggle switch. By contrast, an oscillatory circuit, the repressilator, is only weakly affected by the division cycle. article_number: '066003' author: - first_name: Veronika full_name: Bierbaum, Veronika id: 3FD04378-F248-11E8-B48F-1D18A9856A87 last_name: Bierbaum - first_name: Stefan full_name: Klumpp, Stefan last_name: Klumpp citation: ama: Bierbaum V, Klumpp S. Impact of the cell division cycle on gene circuits. Physical Biology. 2015;12(6). doi:10.1088/1478-3975/12/6/066003 apa: Bierbaum, V., & Klumpp, S. (2015). Impact of the cell division cycle on gene circuits. Physical Biology. IOP Publishing Ltd. https://doi.org/10.1088/1478-3975/12/6/066003 chicago: Bierbaum, Veronika, and Stefan Klumpp. “Impact of the Cell Division Cycle on Gene Circuits.” Physical Biology. IOP Publishing Ltd., 2015. https://doi.org/10.1088/1478-3975/12/6/066003. ieee: V. Bierbaum and S. Klumpp, “Impact of the cell division cycle on gene circuits,” Physical Biology, vol. 12, no. 6. IOP Publishing Ltd., 2015. ista: Bierbaum V, Klumpp S. 2015. Impact of the cell division cycle on gene circuits. Physical Biology. 12(6), 066003. mla: Bierbaum, Veronika, and Stefan Klumpp. “Impact of the Cell Division Cycle on Gene Circuits.” Physical Biology, vol. 12, no. 6, 066003, IOP Publishing Ltd., 2015, doi:10.1088/1478-3975/12/6/066003. short: V. Bierbaum, S. Klumpp, Physical Biology 12 (2015). date_created: 2018-12-11T11:52:33Z date_published: 2015-09-25T00:00:00Z date_updated: 2021-01-12T06:51:25Z day: '25' department: - _id: MiSi doi: 10.1088/1478-3975/12/6/066003 intvolume: ' 12' issue: '6' language: - iso: eng month: '09' oa_version: None publication: Physical Biology publication_status: published publisher: IOP Publishing Ltd. publist_id: '5641' quality_controlled: '1' scopus_import: 1 status: public title: Impact of the cell division cycle on gene circuits type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 12 year: '2015' ... --- _id: '1553' abstract: - lang: eng text: Cell movement has essential functions in development, immunity, and cancer. Various cell migration patterns have been reported, but no general rule has emerged so far. Here, we show on the basis of experimental data in vitro and in vivo that cell persistence, which quantifies the straightness of trajectories, is robustly coupled to cell migration speed. We suggest that this universal coupling constitutes a generic law of cell migration, which originates in the advection of polarity cues by an actin cytoskeleton undergoing flows at the cellular scale. Our analysis relies on a theoretical model that we validate by measuring the persistence of cells upon modulation of actin flow speeds and upon optogenetic manipulation of the binding of an actin regulator to actin filaments. Beyond the quantitative prediction of the coupling, the model yields a generic phase diagram of cellular trajectories, which recapitulates the full range of observed migration patterns. author: - first_name: Paolo full_name: Maiuri, Paolo last_name: Maiuri - first_name: Jean full_name: Rupprecht, Jean last_name: Rupprecht - first_name: Stefan full_name: Wieser, Stefan id: 355AA5A0-F248-11E8-B48F-1D18A9856A87 last_name: Wieser orcid: 0000-0002-2670-2217 - first_name: Verena full_name: Ruprecht, Verena id: 4D71A03A-F248-11E8-B48F-1D18A9856A87 last_name: Ruprecht orcid: 0000-0003-4088-8633 - first_name: Olivier full_name: Bénichou, Olivier last_name: Bénichou - first_name: Nicolas full_name: Carpi, Nicolas last_name: Carpi - first_name: Mathieu full_name: Coppey, Mathieu last_name: Coppey - first_name: Simon full_name: De Beco, Simon last_name: De Beco - first_name: Nir full_name: Gov, Nir last_name: Gov - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 - first_name: Carolina full_name: Lage Crespo, Carolina last_name: Lage Crespo - first_name: Franziska full_name: Lautenschlaeger, Franziska last_name: Lautenschlaeger - first_name: Maël full_name: Le Berre, Maël last_name: Le Berre - first_name: Ana full_name: Lennon Duménil, Ana last_name: Lennon Duménil - first_name: Matthew full_name: Raab, Matthew last_name: Raab - first_name: Hawa full_name: Thiam, Hawa last_name: Thiam - first_name: Matthieu full_name: Piel, Matthieu last_name: Piel - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Raphaël full_name: Voituriez, Raphaël last_name: Voituriez citation: ama: Maiuri P, Rupprecht J, Wieser S, et al. Actin flows mediate a universal coupling between cell speed and cell persistence. Cell. 2015;161(2):374-386. doi:10.1016/j.cell.2015.01.056 apa: Maiuri, P., Rupprecht, J., Wieser, S., Ruprecht, V., Bénichou, O., Carpi, N., … Voituriez, R. (2015). Actin flows mediate a universal coupling between cell speed and cell persistence. Cell. Cell Press. https://doi.org/10.1016/j.cell.2015.01.056 chicago: Maiuri, Paolo, Jean Rupprecht, Stefan Wieser, Verena Ruprecht, Olivier Bénichou, Nicolas Carpi, Mathieu Coppey, et al. “Actin Flows Mediate a Universal Coupling between Cell Speed and Cell Persistence.” Cell. Cell Press, 2015. https://doi.org/10.1016/j.cell.2015.01.056. ieee: P. Maiuri et al., “Actin flows mediate a universal coupling between cell speed and cell persistence,” Cell, vol. 161, no. 2. Cell Press, pp. 374–386, 2015. ista: Maiuri P, Rupprecht J, Wieser S, Ruprecht V, Bénichou O, Carpi N, Coppey M, De Beco S, Gov N, Heisenberg C-PJ, Lage Crespo C, Lautenschlaeger F, Le Berre M, Lennon Duménil A, Raab M, Thiam H, Piel M, Sixt MK, Voituriez R. 2015. Actin flows mediate a universal coupling between cell speed and cell persistence. Cell. 161(2), 374–386. mla: Maiuri, Paolo, et al. “Actin Flows Mediate a Universal Coupling between Cell Speed and Cell Persistence.” Cell, vol. 161, no. 2, Cell Press, 2015, pp. 374–86, doi:10.1016/j.cell.2015.01.056. short: P. Maiuri, J. Rupprecht, S. Wieser, V. Ruprecht, O. Bénichou, N. Carpi, M. Coppey, S. De Beco, N. Gov, C.-P.J. Heisenberg, C. Lage Crespo, F. Lautenschlaeger, M. Le Berre, A. Lennon Duménil, M. Raab, H. Thiam, M. Piel, M.K. Sixt, R. Voituriez, Cell 161 (2015) 374–386. date_created: 2018-12-11T11:52:41Z date_published: 2015-04-09T00:00:00Z date_updated: 2021-01-12T06:51:33Z day: '09' department: - _id: MiSi - _id: CaHe doi: 10.1016/j.cell.2015.01.056 ec_funded: 1 intvolume: ' 161' issue: '2' language: - iso: eng month: '04' oa_version: None page: 374 - 386 project: - _id: 2529486C-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T 560-B17 name: Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25ABD200-B435-11E9-9278-68D0E5697425 grant_number: RGP0058/2011 name: 'Cell migration in complex environments: from in vivo experiments to theoretical models' publication: Cell publication_status: published publisher: Cell Press publist_id: '5618' quality_controlled: '1' scopus_import: 1 status: public title: Actin flows mediate a universal coupling between cell speed and cell persistence type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 161 year: '2015' ... --- _id: '1561' abstract: - lang: eng text: Replication-deficient recombinant adenoviruses are potent vectors for the efficient transient expression of exogenous genes in resting immune cells. However, most leukocytes are refractory to efficient adenoviral transduction as they lack expression of the coxsackie/adenovirus receptor (CAR). To circumvent this obstacle, we generated the R26/CAG-CARΔ1StopF (where R26 is ROSA26 and CAG is CMV early enhancer/chicken β actin promoter) knock-in mouse line. This strain allows monitoring of in situ Cre recombinase activity through expression of CARΔ1. Simultaneously, CARΔ1 expression permits selective and highly efficient adenoviral transduction of immune cell populations, such as mast cells or T cells, directly ex vivo in bulk cultures without prior cell purification or activation. Furthermore, we show that CARΔ1 expression dramatically improves adenoviral infection of in vitro differentiated conventional and plasmacytoid dendritic cells (DCs), basophils, mast cells, as well as Hoxb8-immortalized hematopoietic progenitor cells. This novel dual function mouse strain will hence be a valuable tool to rapidly dissect the function of specific genes in leukocyte physiology. author: - first_name: Klaus full_name: Heger, Klaus last_name: Heger - first_name: Maike full_name: Kober, Maike last_name: Kober - first_name: David full_name: Rieß, David last_name: Rieß - first_name: Christoph full_name: Drees, Christoph last_name: Drees - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Arianna full_name: Bertossi, Arianna last_name: Bertossi - first_name: Axel full_name: Roers, Axel last_name: Roers - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Marc full_name: Schmidt Supprian, Marc last_name: Schmidt Supprian citation: ama: Heger K, Kober M, Rieß D, et al. A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors. European Journal of Immunology. 2015;45(6):1614-1620. doi:10.1002/eji.201545457 apa: Heger, K., Kober, M., Rieß, D., Drees, C., de Vries, I., Bertossi, A., … Schmidt Supprian, M. (2015). A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors. European Journal of Immunology. Wiley. https://doi.org/10.1002/eji.201545457 chicago: Heger, Klaus, Maike Kober, David Rieß, Christoph Drees, Ingrid de Vries, Arianna Bertossi, Axel Roers, Michael K Sixt, and Marc Schmidt Supprian. “A Novel Cre Recombinase Reporter Mouse Strain Facilitates Selective and Efficient Infection of Primary Immune Cells with Adenoviral Vectors.” European Journal of Immunology. Wiley, 2015. https://doi.org/10.1002/eji.201545457. ieee: K. Heger et al., “A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors,” European Journal of Immunology, vol. 45, no. 6. Wiley, pp. 1614–1620, 2015. ista: Heger K, Kober M, Rieß D, Drees C, de Vries I, Bertossi A, Roers A, Sixt MK, Schmidt Supprian M. 2015. A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors. European Journal of Immunology. 45(6), 1614–1620. mla: Heger, Klaus, et al. “A Novel Cre Recombinase Reporter Mouse Strain Facilitates Selective and Efficient Infection of Primary Immune Cells with Adenoviral Vectors.” European Journal of Immunology, vol. 45, no. 6, Wiley, 2015, pp. 1614–20, doi:10.1002/eji.201545457. short: K. Heger, M. Kober, D. Rieß, C. Drees, I. de Vries, A. Bertossi, A. Roers, M.K. Sixt, M. Schmidt Supprian, European Journal of Immunology 45 (2015) 1614–1620. date_created: 2018-12-11T11:52:44Z date_published: 2015-06-01T00:00:00Z date_updated: 2021-01-12T06:51:36Z day: '01' department: - _id: MiSi doi: 10.1002/eji.201545457 intvolume: ' 45' issue: '6' language: - iso: eng month: '06' oa_version: None page: 1614 - 1620 publication: European Journal of Immunology publication_status: published publisher: Wiley publist_id: '5610' quality_controlled: '1' scopus_import: 1 status: public title: A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 45 year: '2015' ... --- _id: '1560' abstract: - lang: eng text: Stromal cells in the subcapsular sinus of the lymph node 'decide' which cells and molecules are allowed access to the deeper parenchyma. The glycoprotein PLVAP is a crucial component of this selector function. author: - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Hons M, Sixt MK. The lymph node filter revealed. Nature Immunology. 2015;16(4):338-340. doi:10.1038/ni.3126 apa: Hons, M., & Sixt, M. K. (2015). The lymph node filter revealed. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3126 chicago: Hons, Miroslav, and Michael K Sixt. “The Lymph Node Filter Revealed.” Nature Immunology. Nature Publishing Group, 2015. https://doi.org/10.1038/ni.3126. ieee: M. Hons and M. K. Sixt, “The lymph node filter revealed,” Nature Immunology, vol. 16, no. 4. Nature Publishing Group, pp. 338–340, 2015. ista: Hons M, Sixt MK. 2015. The lymph node filter revealed. Nature Immunology. 16(4), 338–340. mla: Hons, Miroslav, and Michael K. Sixt. “The Lymph Node Filter Revealed.” Nature Immunology, vol. 16, no. 4, Nature Publishing Group, 2015, pp. 338–40, doi:10.1038/ni.3126. short: M. Hons, M.K. Sixt, Nature Immunology 16 (2015) 338–340. date_created: 2018-12-11T11:52:43Z date_published: 2015-03-19T00:00:00Z date_updated: 2021-01-12T06:51:36Z day: '19' department: - _id: MiSi doi: 10.1038/ni.3126 intvolume: ' 16' issue: '4' language: - iso: eng month: '03' oa_version: None page: 338 - 340 publication: Nature Immunology publication_status: published publisher: Nature Publishing Group publist_id: '5611' quality_controlled: '1' scopus_import: 1 status: public title: The lymph node filter revealed type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 16 year: '2015' ... --- _id: '1575' abstract: - lang: eng text: The immune response relies on the migration of leukocytes and on their ability to stop in precise anatomical locations to fulfil their task. How leukocyte migration and function are coordinated is unknown. Here we show that in immature dendritic cells, which patrol their environment by engulfing extracellular material, cell migration and antigen capture are antagonistic. This antagonism results from transient enrichment of myosin IIA at the cell front, which disrupts the back-to-front gradient of the motor protein, slowing down locomotion but promoting antigen capture. We further highlight that myosin IIA enrichment at the cell front requires the MHC class II-associated invariant chain (Ii). Thus, by controlling myosin IIA localization, Ii imposes on dendritic cells an intermittent antigen capture behaviour that might facilitate environment patrolling. We propose that the requirement for myosin II in both cell migration and specific cell functions may provide a general mechanism for their coordination in time and space. acknowledgement: M.C. and M.L.H. were supported by fellowships from the Fondation pour la Recherche Médicale and the Association pour la Recherche contre le Cancer, respectively. This work was funded by grants from the City of Paris and the European Research Council to A.-M.L.-D. (Strapacemi 243103), the Association Nationale pour la Recherche (ANR-09-PIRI-0027-PCVI) and the InnaBiosanté foundation (Micemico) to A.-M.L.-D., M.P. and R.V., and the DCBIOL Labex from the French Government (ANR-10-IDEX-0001-02-PSL* and ANR-11-LABX-0043). The super-resolution SIM microscope was funded through an ERC Advanced Investigator Grant (250367) to Edith Heard (CNRS UMR3215/Inserm U934, Institut Curie). article_number: '7526' author: - first_name: Mélanie full_name: Chabaud, Mélanie last_name: Chabaud - first_name: Mélina full_name: Heuzé, Mélina last_name: Heuzé - first_name: Marine full_name: Bretou, Marine last_name: Bretou - first_name: Pablo full_name: Vargas, Pablo last_name: Vargas - first_name: Paolo full_name: Maiuri, Paolo last_name: Maiuri - first_name: Paola full_name: Solanes, Paola last_name: Solanes - first_name: Mathieu full_name: Maurin, Mathieu last_name: Maurin - first_name: Emmanuel full_name: Terriac, Emmanuel last_name: Terriac - first_name: Maël full_name: Le Berre, Maël last_name: Le Berre - first_name: Danielle full_name: Lankar, Danielle last_name: Lankar - first_name: Tristan full_name: Piolot, Tristan last_name: Piolot - first_name: Robert full_name: Adelstein, Robert last_name: Adelstein - first_name: Yingfan full_name: Zhang, Yingfan last_name: Zhang - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Jordan full_name: Jacobelli, Jordan last_name: Jacobelli - first_name: Olivier full_name: Bénichou, Olivier last_name: Bénichou - first_name: Raphaël full_name: Voituriez, Raphaël last_name: Voituriez - first_name: Matthieu full_name: Piel, Matthieu last_name: Piel - first_name: Ana full_name: Lennon Duménil, Ana last_name: Lennon Duménil citation: ama: Chabaud M, Heuzé M, Bretou M, et al. Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells. Nature Communications. 2015;6. doi:10.1038/ncomms8526 apa: Chabaud, M., Heuzé, M., Bretou, M., Vargas, P., Maiuri, P., Solanes, P., … Lennon Duménil, A. (2015). Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms8526 chicago: Chabaud, Mélanie, Mélina Heuzé, Marine Bretou, Pablo Vargas, Paolo Maiuri, Paola Solanes, Mathieu Maurin, et al. “Cell Migration and Antigen Capture Are Antagonistic Processes Coupled by Myosin II in Dendritic Cells.” Nature Communications. Nature Publishing Group, 2015. https://doi.org/10.1038/ncomms8526. ieee: M. Chabaud et al., “Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells,” Nature Communications, vol. 6. Nature Publishing Group, 2015. ista: Chabaud M, Heuzé M, Bretou M, Vargas P, Maiuri P, Solanes P, Maurin M, Terriac E, Le Berre M, Lankar D, Piolot T, Adelstein R, Zhang Y, Sixt MK, Jacobelli J, Bénichou O, Voituriez R, Piel M, Lennon Duménil A. 2015. Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells. Nature Communications. 6, 7526. mla: Chabaud, Mélanie, et al. “Cell Migration and Antigen Capture Are Antagonistic Processes Coupled by Myosin II in Dendritic Cells.” Nature Communications, vol. 6, 7526, Nature Publishing Group, 2015, doi:10.1038/ncomms8526. short: M. Chabaud, M. Heuzé, M. Bretou, P. Vargas, P. Maiuri, P. Solanes, M. Maurin, E. Terriac, M. Le Berre, D. Lankar, T. Piolot, R. Adelstein, Y. Zhang, M.K. Sixt, J. Jacobelli, O. Bénichou, R. Voituriez, M. Piel, A. Lennon Duménil, Nature Communications 6 (2015). date_created: 2018-12-11T11:52:48Z date_published: 2015-06-25T00:00:00Z date_updated: 2021-01-12T06:51:42Z day: '25' ddc: - '570' department: - _id: MiSi doi: 10.1038/ncomms8526 file: - access_level: open_access checksum: bae12e86be2adb28253f890b8bba8315 content_type: application/pdf creator: system date_created: 2018-12-12T10:11:58Z date_updated: 2020-07-14T12:45:02Z file_id: '4915' file_name: IST-2016-476-v1+1_ncomms8526.pdf file_size: 4530215 relation: main_file file_date_updated: 2020-07-14T12:45:02Z has_accepted_license: '1' intvolume: ' 6' language: - iso: eng month: '06' oa: 1 oa_version: Published Version publication: Nature Communications publication_status: published publisher: Nature Publishing Group publist_id: '5596' pubrep_id: '476' quality_controlled: '1' scopus_import: 1 status: public title: Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 6 year: '2015' ... --- _id: '1676' author: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Erez full_name: Raz, Erez last_name: Raz citation: ama: 'Sixt MK, Raz E. Editorial overview: Cell adhesion and migration. Current Opinion in Cell Biology. 2015;36(10):4-6. doi:10.1016/j.ceb.2015.09.004' apa: 'Sixt, M. K., & Raz, E. (2015). Editorial overview: Cell adhesion and migration. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2015.09.004' chicago: 'Sixt, Michael K, and Erez Raz. “Editorial Overview: Cell Adhesion and Migration.” Current Opinion in Cell Biology. Elsevier, 2015. https://doi.org/10.1016/j.ceb.2015.09.004.' ieee: 'M. K. Sixt and E. Raz, “Editorial overview: Cell adhesion and migration,” Current Opinion in Cell Biology, vol. 36, no. 10. Elsevier, pp. 4–6, 2015.' ista: 'Sixt MK, Raz E. 2015. Editorial overview: Cell adhesion and migration. Current Opinion in Cell Biology. 36(10), 4–6.' mla: 'Sixt, Michael K., and Erez Raz. “Editorial Overview: Cell Adhesion and Migration.” Current Opinion in Cell Biology, vol. 36, no. 10, Elsevier, 2015, pp. 4–6, doi:10.1016/j.ceb.2015.09.004.' short: M.K. Sixt, E. Raz, Current Opinion in Cell Biology 36 (2015) 4–6. date_created: 2018-12-11T11:53:25Z date_published: 2015-10-01T00:00:00Z date_updated: 2021-01-12T06:52:27Z day: '01' department: - _id: MiSi doi: 10.1016/j.ceb.2015.09.004 intvolume: ' 36' issue: '10' language: - iso: eng month: '10' oa_version: None page: 4 - 6 publication: Current Opinion in Cell Biology publication_status: published publisher: Elsevier publist_id: '5473' scopus_import: 1 status: public title: 'Editorial overview: Cell adhesion and migration' type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 36 year: '2015' ... --- _id: '1687' abstract: - lang: eng text: Guided cell movement is essential for development and integrity of animals and crucially involved in cellular immune responses. Leukocytes are professional migratory cells that can navigate through most types of tissues and sense a wide range of directional cues. The responses of these cells to attractants have been mainly explored in tissue culture settings. How leukocytes make directional decisions in situ, within the challenging environment of a tissue maze, is less understood. Here we review recent advances in how leukocytes sense chemical cues in complex tissue settings and make links with paradigms of directed migration in development and Dictyostelium discoideum amoebae. author: - first_name: Milka full_name: Sarris, Milka last_name: Sarris - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Sarris M, Sixt MK. Navigating in tissue mazes: Chemoattractant interpretation in complex environments. Current Opinion in Cell Biology. 2015;36(10):93-102. doi:10.1016/j.ceb.2015.08.001' apa: 'Sarris, M., & Sixt, M. K. (2015). Navigating in tissue mazes: Chemoattractant interpretation in complex environments. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2015.08.001' chicago: 'Sarris, Milka, and Michael K Sixt. “Navigating in Tissue Mazes: Chemoattractant Interpretation in Complex Environments.” Current Opinion in Cell Biology. Elsevier, 2015. https://doi.org/10.1016/j.ceb.2015.08.001.' ieee: 'M. Sarris and M. K. Sixt, “Navigating in tissue mazes: Chemoattractant interpretation in complex environments,” Current Opinion in Cell Biology, vol. 36, no. 10. Elsevier, pp. 93–102, 2015.' ista: 'Sarris M, Sixt MK. 2015. Navigating in tissue mazes: Chemoattractant interpretation in complex environments. Current Opinion in Cell Biology. 36(10), 93–102.' mla: 'Sarris, Milka, and Michael K. Sixt. “Navigating in Tissue Mazes: Chemoattractant Interpretation in Complex Environments.” Current Opinion in Cell Biology, vol. 36, no. 10, Elsevier, 2015, pp. 93–102, doi:10.1016/j.ceb.2015.08.001.' short: M. Sarris, M.K. Sixt, Current Opinion in Cell Biology 36 (2015) 93–102. date_created: 2018-12-11T11:53:28Z date_published: 2015-10-01T00:00:00Z date_updated: 2021-01-12T06:52:31Z day: '01' ddc: - '570' department: - _id: MiSi doi: 10.1016/j.ceb.2015.08.001 ec_funded: 1 file: - access_level: open_access checksum: c29973924b790aab02fdd91857759cfb content_type: application/pdf creator: system date_created: 2018-12-12T10:11:21Z date_updated: 2020-07-14T12:45:12Z file_id: '4875' file_name: IST-2016-445-v1+1_1-s2.0-S0955067415001064-main.pdf file_size: 797964 relation: main_file file_date_updated: 2020-07-14T12:45:12Z has_accepted_license: '1' intvolume: ' 36' issue: '10' language: - iso: eng month: '10' oa: 1 oa_version: Published Version page: 93 - 102 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Current Opinion in Cell Biology publication_status: published publisher: Elsevier publist_id: '5458' pubrep_id: '445' quality_controlled: '1' scopus_import: 1 status: public title: 'Navigating in tissue mazes: Chemoattractant interpretation in complex environments' tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 36 year: '2015' ... --- _id: '1686' author: - first_name: Eva full_name: Kiermaier, Eva id: 3EB04B78-F248-11E8-B48F-1D18A9856A87 last_name: Kiermaier orcid: 0000-0001-6165-5738 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Kiermaier E, Sixt MK. Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. Science. 2015;349(6252):1055-1056. doi:10.1126/science.aad0867' apa: 'Kiermaier, E., & Sixt, M. K. (2015). Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.aad0867' chicago: 'Kiermaier, Eva, and Michael K Sixt. “Fragmented Communication between Immune Cells: Neutrophils Blaze a Trail with Migratory Cues for T Cells to Follow to Sites of Infection.” Science. American Association for the Advancement of Science, 2015. https://doi.org/10.1126/science.aad0867.' ieee: 'E. Kiermaier and M. K. Sixt, “Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection,” Science, vol. 349, no. 6252. American Association for the Advancement of Science, pp. 1055–1056, 2015.' ista: 'Kiermaier E, Sixt MK. 2015. Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. Science. 349(6252), 1055–1056.' mla: 'Kiermaier, Eva, and Michael K. Sixt. “Fragmented Communication between Immune Cells: Neutrophils Blaze a Trail with Migratory Cues for T Cells to Follow to Sites of Infection.” Science, vol. 349, no. 6252, American Association for the Advancement of Science, 2015, pp. 1055–56, doi:10.1126/science.aad0867.' short: E. Kiermaier, M.K. Sixt, Science 349 (2015) 1055–1056. date_created: 2018-12-11T11:53:28Z date_published: 2015-09-04T00:00:00Z date_updated: 2021-01-12T06:52:31Z day: '04' department: - _id: MiSi doi: 10.1126/science.aad0867 intvolume: ' 349' issue: '6252' language: - iso: eng month: '09' oa_version: None page: 1055 - 1056 publication: Science publication_status: published publisher: American Association for the Advancement of Science publist_id: '5459' quality_controlled: '1' scopus_import: 1 status: public title: 'Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection' type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 349 year: '2015' ... --- _id: '477' abstract: - lang: eng text: Dendritic cells are potent antigen-presenting cells endowed with the unique ability to initiate adaptive immune responses upon inflammation. Inflammatory processes are often associated with an increased production of serotonin, which operates by activating specific receptors. However, the functional role of serotonin receptors in regulation of dendritic cell functions is poorly understood. Here, we demonstrate that expression of serotonin receptor 5-HT7 (5-HT7TR) as well as its downstream effector Cdc42 is upregulated in dendritic cells upon maturation. Although dendritic cell maturation was independent of 5-HT7TR, receptor stimulation affected dendritic cell morphology through Cdc42-mediated signaling. In addition, basal activity of 5-HT7TR was required for the proper expression of the chemokine receptor CCR7, which is a key factor that controls dendritic cell migration. Consistent with this, we observed that 5-HT7TR enhances chemotactic motility of dendritic cells in vitro by modulating their directionality and migration velocity. Accordingly, migration of dendritic cells in murine colon explants was abolished after pharmacological receptor inhibition. Our results indicate that there is a crucial role for 5-HT7TR-Cdc42-mediated signaling in the regulation of dendritic cell morphology and motility, suggesting that 5-HT7TR could be a new target for treatment of a variety of inflammatory and immune disorders. author: - first_name: Katrin full_name: Holst, Katrin last_name: Holst - first_name: Daria full_name: Guseva, Daria last_name: Guseva - first_name: Susann full_name: Schindler, Susann last_name: Schindler - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Armin full_name: Braun, Armin last_name: Braun - first_name: Himpriya full_name: Chopra, Himpriya last_name: Chopra - first_name: Oliver full_name: Pabst, Oliver last_name: Pabst - first_name: Evgeni full_name: Ponimaskin, Evgeni last_name: Ponimaskin citation: ama: Holst K, Guseva D, Schindler S, et al. The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. Journal of Cell Science. 2015;128(15):2866-2880. doi:10.1242/jcs.167999 apa: Holst, K., Guseva, D., Schindler, S., Sixt, M. K., Braun, A., Chopra, H., … Ponimaskin, E. (2015). The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.167999 chicago: Holst, Katrin, Daria Guseva, Susann Schindler, Michael K Sixt, Armin Braun, Himpriya Chopra, Oliver Pabst, and Evgeni Ponimaskin. “The Serotonin Receptor 5-HT7R Regulates the Morphology and Migratory Properties of Dendritic Cells.” Journal of Cell Science. Company of Biologists, 2015. https://doi.org/10.1242/jcs.167999. ieee: K. Holst et al., “The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells,” Journal of Cell Science, vol. 128, no. 15. Company of Biologists, pp. 2866–2880, 2015. ista: Holst K, Guseva D, Schindler S, Sixt MK, Braun A, Chopra H, Pabst O, Ponimaskin E. 2015. The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. Journal of Cell Science. 128(15), 2866–2880. mla: Holst, Katrin, et al. “The Serotonin Receptor 5-HT7R Regulates the Morphology and Migratory Properties of Dendritic Cells.” Journal of Cell Science, vol. 128, no. 15, Company of Biologists, 2015, pp. 2866–80, doi:10.1242/jcs.167999. short: K. Holst, D. Guseva, S. Schindler, M.K. Sixt, A. Braun, H. Chopra, O. Pabst, E. Ponimaskin, Journal of Cell Science 128 (2015) 2866–2880. date_created: 2018-12-11T11:46:41Z date_published: 2015-06-15T00:00:00Z date_updated: 2021-01-12T08:00:54Z day: '15' department: - _id: MiSi doi: 10.1242/jcs.167999 intvolume: ' 128' issue: '15' language: - iso: eng month: '06' oa_version: None page: 2866 - 2880 publication: Journal of Cell Science publication_status: published publisher: Company of Biologists publist_id: '7343' quality_controlled: '1' scopus_import: 1 status: public title: The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 128 year: '2015' ...