[{"isi":1,"article_type":"original","date_updated":"2026-09-28T22:30:17Z","ddc":["570"],"date_created":"2023-09-24T22:01:10Z","file":[{"creator":"dernst","checksum":"ad670e3b3c64fc585675948370f6b149","access_level":"open_access","file_size":2725421,"content_type":"application/pdf","success":1,"date_created":"2023-09-25T08:22:58Z","relation":"main_file","file_name":"2023_NatureComm_Sitarska.pdf","date_updated":"2023-09-25T08:22:58Z","file_id":"14365"}],"citation":{"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).","ama":"Sitarska E, Almeida SD, Beckwith MS, et al. Sensing their plasma membrane curvature allows migrating cells to circumvent obstacles. <i>Nature Communications</i>. 2023;14. doi:<a href=\"https://doi.org/10.1038/s41467-023-41173-1\">10.1038/s41467-023-41173-1</a>","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. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-023-41173-1\">https://doi.org/10.1038/s41467-023-41173-1</a>","mla":"Sitarska, Ewa, et al. “Sensing Their Plasma Membrane Curvature Allows Migrating Cells to Circumvent Obstacles.” <i>Nature Communications</i>, vol. 14, 5644, Springer Nature, 2023, doi:<a href=\"https://doi.org/10.1038/s41467-023-41173-1\">10.1038/s41467-023-41173-1</a>.","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.","ieee":"E. Sitarska <i>et al.</i>, “Sensing their plasma membrane curvature allows migrating cells to circumvent obstacles,” <i>Nature Communications</i>, vol. 14. Springer Nature, 2023.","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.” <i>Nature Communications</i>. Springer Nature, 2023. <a href=\"https://doi.org/10.1038/s41467-023-41173-1\">https://doi.org/10.1038/s41467-023-41173-1</a>."},"oa":1,"year":"2023","type":"journal_article","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"eissn":["2041-1723"]},"oa_version":"Published Version","scopus_import":"1","tmp":{"image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)"},"month":"09","external_id":{"pmid":["37704612"],"isi":["001087583700008"]},"department":[{"_id":"MiSi"}],"status":"public","article_number":"5644","publication":"Nature Communications","language":[{"iso":"eng"}],"related_material":{"record":[{"id":"14697","relation":"dissertation_contains","status":"public"}]},"author":[{"first_name":"Ewa","last_name":"Sitarska","full_name":"Sitarska, Ewa"},{"first_name":"Silvia Dias","last_name":"Almeida","full_name":"Almeida, Silvia Dias"},{"first_name":"Marianne Sandvold","last_name":"Beckwith","full_name":"Beckwith, Marianne Sandvold"},{"id":"489E3F00-F248-11E8-B48F-1D18A9856A87","full_name":"Stopp, Julian A","last_name":"Stopp","first_name":"Julian A"},{"full_name":"Czuchnowski, Jakub","last_name":"Czuchnowski","first_name":"Jakub"},{"last_name":"Siggel","full_name":"Siggel, Marc","first_name":"Marc"},{"full_name":"Roessner, Rita","last_name":"Roessner","first_name":"Rita"},{"first_name":"Aline","full_name":"Tschanz, Aline","last_name":"Tschanz"},{"last_name":"Ejsing","full_name":"Ejsing, Christer","first_name":"Christer"},{"last_name":"Schwab","full_name":"Schwab, Yannick","first_name":"Yannick"},{"last_name":"Kosinski","full_name":"Kosinski, Jan","first_name":"Jan"},{"first_name":"Michael K","last_name":"Sixt","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K"},{"last_name":"Kreshuk","full_name":"Kreshuk, Anna","first_name":"Anna"},{"full_name":"Erzberger, Anna","last_name":"Erzberger","first_name":"Anna"},{"first_name":"Alba","last_name":"Diz-Muñoz","full_name":"Diz-Muñoz, Alba"}],"publication_status":"published","article_processing_charge":"Yes (via OA deal)","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.","intvolume":"        14","title":"Sensing their plasma membrane curvature allows migrating cells to circumvent obstacles","pmid":1,"volume":14,"date_published":"2023-09-13T00:00:00Z","has_accepted_license":"1","fulldoi":"https://doi.org/10.1038/s41467-023-41173-1","day":"13","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."}],"quality_controlled":"1","_id":"14360","license":"https://creativecommons.org/licenses/by/4.0/","publisher":"Springer Nature","file_date_updated":"2023-09-25T08:22:58Z","doi":"10.1038/s41467-023-41173-1"},{"quality_controlled":"1","abstract":[{"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.","lang":"eng"}],"day":"01","fulldoi":"https://doi.org/10.1126/sciimmunol.adc9584","issue":"87","doi":"10.1126/sciimmunol.adc9584","publisher":"American Association for the Advancement of Science","keyword":["General Medicine","Immunology"],"_id":"14274","related_material":{"record":[{"id":"14279","relation":"research_data","status":"public"},{"relation":"dissertation_contains","id":"14697","status":"public"},{"relation":"dissertation_contains","id":"19745","status":"public"}]},"language":[{"iso":"eng"}],"publication":"Science Immunology","article_number":"adc9584","status":"public","ec_funded":1,"department":[{"_id":"MiSi"},{"_id":"EdHa"},{"_id":"NanoFab"}],"pmid":1,"volume":8,"date_published":"2023-09-01T00:00:00Z","title":"CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective leukocyte migration","intvolume":"         8","article_processing_charge":"No","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.","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","orcid":"0000-0003-0506-4217","id":"50B2A802-6007-11E9-A42B-EB23E6697425","last_name":"Ucar"},{"id":"3795523E-F248-11E8-B48F-1D18A9856A87","last_name":"Canigova","full_name":"Canigova, Nikola","orcid":"0000-0002-8518-5926","first_name":"Nikola"},{"last_name":"Stopp","id":"489E3F00-F248-11E8-B48F-1D18A9856A87","full_name":"Stopp, Julian A","first_name":"Julian A"},{"first_name":"Jan","last_name":"Schwarz","id":"346C1EC6-F248-11E8-B48F-1D18A9856A87","full_name":"Schwarz, Jan"},{"id":"4515C308-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5145-4609","last_name":"Merrin","full_name":"Merrin, Jack","first_name":"Jack"},{"full_name":"Hannezo, Edouard B","last_name":"Hannezo","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6005-1561","first_name":"Edouard B"},{"first_name":"Michael K","orcid":"0000-0002-6620-9179","last_name":"Sixt","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"publication_status":"published","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"issn":["2470-9468"]},"type":"journal_article","corr_author":"1","project":[{"grant_number":"724373","name":"Cellular Navigation Along Spatial Gradients","call_identifier":"H2020","_id":"25FE9508-B435-11E9-9278-68D0E5697425"},{"name":"Design Principles of Branching Morphogenesis","grant_number":"851288","call_identifier":"H2020","_id":"05943252-7A3F-11EA-A408-12923DDC885E"},{"_id":"265E2996-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Nano-Analytics of Cellular Systems","grant_number":"W01250-B20"},{"call_identifier":"H2020","grant_number":"754411","name":"ISTplus - Postdoctoral Fellowships","_id":"260C2330-B435-11E9-9278-68D0E5697425"}],"year":"2023","external_id":{"isi":["001062110600003"],"pmid":["37656776"]},"month":"09","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1126/sciimmunol.adc9584"}],"scopus_import":"1","oa_version":"Published Version","ddc":["570"],"date_updated":"2026-09-28T22:30:35Z","article_type":"original","isi":1,"oa":1,"citation":{"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.” <i>Science Immunology</i>, vol. 8, no. 87, adc9584, American Association for the Advancement of Science, 2023, doi:<a href=\"https://doi.org/10.1126/sciimmunol.adc9584\">10.1126/sciimmunol.adc9584</a>.","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. <i>Science Immunology</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/sciimmunol.adc9584\">https://doi.org/10.1126/sciimmunol.adc9584</a>","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. <i>Science Immunology</i>. 2023;8(87). doi:<a href=\"https://doi.org/10.1126/sciimmunol.adc9584\">10.1126/sciimmunol.adc9584</a>","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).","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.” <i>Science Immunology</i>. American Association for the Advancement of Science, 2023. <a href=\"https://doi.org/10.1126/sciimmunol.adc9584\">https://doi.org/10.1126/sciimmunol.adc9584</a>.","ieee":"J. H. Alanko <i>et al.</i>, “CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective leukocyte migration,” <i>Science Immunology</i>, vol. 8, no. 87. American Association for the Advancement of Science, 2023."},"date_created":"2023-09-06T08:07:51Z"},{"corr_author":"1","type":"journal_article","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","publication_identifier":{"issn":["0390-6078"],"eissn":["1592-8721"]},"project":[{"name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells","grant_number":"747687","call_identifier":"H2020","_id":"260AA4E2-B435-11E9-9278-68D0E5697425"}],"year":"2022","month":"07","external_id":{"isi":["000823746100018"]},"oa_version":"Published Version","scopus_import":"1","tmp":{"short":"CC BY-NC (4.0)","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)","image":"/images/cc_by_nc.png"},"ddc":["570"],"article_type":"original","isi":1,"date_updated":"2025-04-14T07:43:16Z","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. <i>Haematologica</i>. 2022;107(7):1669-1680. doi:<a href=\"https://doi.org/10.3324/haematol.2021.278896\">10.3324/haematol.2021.278896</a>","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.","mla":"Nicolai, Leo, et al. “Single Platelet and Megakaryocyte Morpho-Dynamics Uncovered by Multicolor Reporter Mouse Strains in Vitro and in Vivo.” <i>Haematologica</i>, vol. 107, no. 7, Ferrata Storti Foundation, 2022, pp. 1669–80, doi:<a href=\"https://doi.org/10.3324/haematol.2021.278896\">10.3324/haematol.2021.278896</a>.","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. <i>Haematologica</i>. Ferrata Storti Foundation. <a href=\"https://doi.org/10.3324/haematol.2021.278896\">https://doi.org/10.3324/haematol.2021.278896</a>","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.","ieee":"L. Nicolai <i>et al.</i>, “Single platelet and megakaryocyte morpho-dynamics uncovered by multicolor reporter mouse strains in vitro and in vivo,” <i>Haematologica</i>, vol. 107, no. 7. Ferrata Storti Foundation, pp. 1669–1680, 2022.","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.” <i>Haematologica</i>. Ferrata Storti Foundation, 2022. <a href=\"https://doi.org/10.3324/haematol.2021.278896\">https://doi.org/10.3324/haematol.2021.278896</a>."},"oa":1,"date_created":"2022-07-17T22:01:54Z","file":[{"relation":"main_file","file_id":"11595","date_updated":"2022-07-18T07:51:55Z","file_name":"2022_Haematologica_Nicolai.pdf","checksum":"9b47830945f3c30428fe9cfee2dc4a8a","creator":"dernst","date_created":"2022-07-18T07:51:55Z","success":1,"file_size":1722094,"content_type":"application/pdf","access_level":"open_access"}],"day":"01","abstract":[{"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.","lang":"eng"}],"quality_controlled":"1","issue":"7","fulldoi":"https://doi.org/10.3324/haematol.2021.278896","has_accepted_license":"1","publisher":"Ferrata Storti Foundation","doi":"10.3324/haematol.2021.278896","file_date_updated":"2022-07-18T07:51:55Z","license":"https://creativecommons.org/licenses/by-nc/4.0/","_id":"11588","language":[{"iso":"eng"}],"department":[{"_id":"MiSi"}],"ec_funded":1,"page":"1669-1680","status":"public","publication":"Haematologica","date_published":"2022-07-01T00:00:00Z","volume":107,"author":[{"first_name":"Leo","full_name":"Nicolai, Leo","last_name":"Nicolai"},{"full_name":"Kaiser, Rainer","last_name":"Kaiser","first_name":"Rainer"},{"full_name":"Escaig, Raphael","last_name":"Escaig","first_name":"Raphael"},{"first_name":"Marie Louise","full_name":"Hoffknecht, Marie Louise","last_name":"Hoffknecht"},{"first_name":"Afra","last_name":"Anjum","full_name":"Anjum, Afra"},{"full_name":"Leunig, Alexander","last_name":"Leunig","first_name":"Alexander"},{"first_name":"Joachim","last_name":"Pircher","full_name":"Pircher, Joachim"},{"full_name":"Ehrlich, Andreas","last_name":"Ehrlich","first_name":"Andreas"},{"first_name":"Michael","full_name":"Lorenz, Michael","last_name":"Lorenz"},{"last_name":"Ishikawa-Ankerhold","full_name":"Ishikawa-Ankerhold, Hellen","first_name":"Hellen"},{"last_name":"Aird","full_name":"Aird, William C.","first_name":"William C."},{"last_name":"Massberg","full_name":"Massberg, Steffen","first_name":"Steffen"},{"first_name":"Florian R","last_name":"Gärtner","id":"397A88EE-F248-11E8-B48F-1D18A9856A87","full_name":"Gärtner, Florian R","orcid":"0000-0001-6120-3723"}],"publication_status":"published","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","title":"Single platelet and megakaryocyte morpho-dynamics uncovered by multicolor reporter mouse strains in vitro and in vivo","intvolume":"       107"},{"type":"journal_article","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","publication_identifier":{"eissn":["1476-4660"],"issn":["1476-1122"]},"year":"2022","month":"09","external_id":{"pmid":["36008604"],"isi":["000844592000002"]},"scopus_import":"1","oa_version":"Preprint","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1101/2020.07.27.219618"}],"article_type":"original","isi":1,"date_updated":"2023-08-03T14:08:47Z","oa":1,"citation":{"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.” <i>Nature Materials</i>. Springer Nature, 2022. <a href=\"https://doi.org/10.1038/s41563-022-01288-0\">https://doi.org/10.1038/s41563-022-01288-0</a>.","ieee":"Y. Mulla <i>et al.</i>, “Weak catch bonds make strong networks,” <i>Nature Materials</i>, vol. 21, no. 9. Springer Nature, pp. 1019–1023, 2022.","mla":"Mulla, Yuval, et al. “Weak Catch Bonds Make Strong Networks.” <i>Nature Materials</i>, vol. 21, no. 9, Springer Nature, 2022, pp. 1019–23, doi:<a href=\"https://doi.org/10.1038/s41563-022-01288-0\">10.1038/s41563-022-01288-0</a>.","apa":"Mulla, Y., Avellaneda Sarrió, M., Roland, A., Baldauf, L., Jung, W., Kim, T., … Koenderink, G. H. (2022). Weak catch bonds make strong networks. <i>Nature Materials</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41563-022-01288-0\">https://doi.org/10.1038/s41563-022-01288-0</a>","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.","ama":"Mulla Y, Avellaneda Sarrió M, Roland A, et al. Weak catch bonds make strong networks. <i>Nature Materials</i>. 2022;21(9):1019-1023. doi:<a href=\"https://doi.org/10.1038/s41563-022-01288-0\">10.1038/s41563-022-01288-0</a>","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","abstract":[{"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.","lang":"eng"}],"day":"01","quality_controlled":"1","fulldoi":"https://doi.org/10.1038/s41563-022-01288-0","issue":"9","doi":"10.1038/s41563-022-01288-0","publisher":"Springer Nature","_id":"12085","language":[{"iso":"eng"}],"department":[{"_id":"MiSi"}],"publication":"Nature Materials","status":"public","page":"1019-1023","pmid":1,"date_published":"2022-09-01T00:00:00Z","volume":21,"author":[{"full_name":"Mulla, Yuval","last_name":"Mulla","first_name":"Yuval"},{"first_name":"Mario","orcid":"0000-0001-6406-524X","full_name":"Avellaneda Sarrió, Mario","last_name":"Avellaneda Sarrió","id":"DC4BA84C-56E6-11EA-AD5D-348C3DDC885E"},{"first_name":"Antoine","last_name":"Roland","full_name":"Roland, Antoine"},{"first_name":"Lucia","last_name":"Baldauf","full_name":"Baldauf, Lucia"},{"last_name":"Jung","full_name":"Jung, Wonyeong","first_name":"Wonyeong"},{"full_name":"Kim, Taeyoon","last_name":"Kim","first_name":"Taeyoon"},{"last_name":"Tans","full_name":"Tans, Sander J.","first_name":"Sander J."},{"first_name":"Gijsje H.","last_name":"Koenderink","full_name":"Koenderink, Gijsje H."}],"publication_status":"published","intvolume":"        21","title":"Weak catch bonds make strong networks","article_processing_charge":"No","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.)."},{"_id":"12119","license":"https://creativecommons.org/licenses/by-nc-nd/4.0/","keyword":["Infectious Diseases","Immunology","Immunology and Allergy"],"file_date_updated":"2023-01-23T10:18:48Z","doi":"10.1016/j.immuni.2022.10.001","publisher":"Elsevier","has_accepted_license":"1","fulldoi":"https://doi.org/10.1016/j.immuni.2022.10.001","issue":"12","abstract":[{"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.","lang":"eng"}],"day":"13","quality_controlled":"1","publication_status":"published","author":[{"first_name":"Tobias","full_name":"Petzold, Tobias","last_name":"Petzold"},{"first_name":"Zhe","last_name":"Zhang","full_name":"Zhang, Zhe"},{"last_name":"Ballesteros","full_name":"Ballesteros, Iván","first_name":"Iván"},{"last_name":"Saleh","full_name":"Saleh, Inas","first_name":"Inas"},{"last_name":"Polzin","full_name":"Polzin, Amin","first_name":"Amin"},{"last_name":"Thienel","full_name":"Thienel, Manuela","first_name":"Manuela"},{"first_name":"Lulu","full_name":"Liu, Lulu","last_name":"Liu"},{"first_name":"Qurrat","full_name":"Ul Ain, Qurrat","last_name":"Ul Ain"},{"full_name":"Ehreiser, Vincent","last_name":"Ehreiser","first_name":"Vincent"},{"last_name":"Weber","full_name":"Weber, Christian","first_name":"Christian"},{"first_name":"Badr","full_name":"Kilani, Badr","last_name":"Kilani"},{"last_name":"Mertsch","full_name":"Mertsch, Pontus","first_name":"Pontus"},{"first_name":"Jeremias","last_name":"Götschke","full_name":"Götschke, Jeremias"},{"first_name":"Sophie","full_name":"Cremer, Sophie","last_name":"Cremer"},{"first_name":"Wenwen","full_name":"Fu, Wenwen","last_name":"Fu"},{"full_name":"Lorenz, Michael","last_name":"Lorenz","first_name":"Michael"},{"first_name":"Hellen","full_name":"Ishikawa-Ankerhold, Hellen","last_name":"Ishikawa-Ankerhold"},{"last_name":"Raatz","full_name":"Raatz, Elisabeth","first_name":"Elisabeth"},{"full_name":"El-Nemr, Shaza","last_name":"El-Nemr","first_name":"Shaza"},{"full_name":"Görlach, Agnes","last_name":"Görlach","first_name":"Agnes"},{"full_name":"Marhuenda, Esther","last_name":"Marhuenda","first_name":"Esther"},{"first_name":"Konstantin","last_name":"Stark","full_name":"Stark, Konstantin"},{"first_name":"Joachim","last_name":"Pircher","full_name":"Pircher, Joachim"},{"first_name":"David","last_name":"Stegner","full_name":"Stegner, David"},{"full_name":"Gieger, Christian","last_name":"Gieger","first_name":"Christian"},{"first_name":"Marc","full_name":"Schmidt-Supprian, Marc","last_name":"Schmidt-Supprian"},{"id":"397A88EE-F248-11E8-B48F-1D18A9856A87","full_name":"Gärtner, Florian R","last_name":"Gärtner","orcid":"0000-0001-6120-3723","first_name":"Florian R"},{"last_name":"Almendros","full_name":"Almendros, Isaac","first_name":"Isaac"},{"full_name":"Kelm, Malte","last_name":"Kelm","first_name":"Malte"},{"full_name":"Schulz, Christian","last_name":"Schulz","first_name":"Christian"},{"first_name":"Andrés","last_name":"Hidalgo","full_name":"Hidalgo, Andrés"},{"full_name":"Massberg, Steffen","last_name":"Massberg","first_name":"Steffen"}],"title":"Neutrophil “plucking” on megakaryocytes drives platelet production and boosts cardiovascular disease","intvolume":"        55","article_processing_charge":"No","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.","pmid":1,"date_published":"2022-12-13T00:00:00Z","volume":55,"ec_funded":1,"department":[{"_id":"MiSi"}],"publication":"Immunity","status":"public","page":"2285-2299.e7","language":[{"iso":"eng"}],"tmp":{"image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)"},"scopus_import":"1","oa_version":"Published Version","month":"12","external_id":{"isi":["000922019600003"],"pmid":["36272416"]},"project":[{"name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells","grant_number":"747687","call_identifier":"H2020","_id":"260AA4E2-B435-11E9-9278-68D0E5697425"}],"year":"2022","type":"journal_article","publication_identifier":{"issn":["1074-7613"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","date_created":"2023-01-12T11:56:54Z","file":[{"date_updated":"2023-01-23T10:18:48Z","file_id":"12341","file_name":"2022_Immunity_Petzold.pdf","relation":"main_file","date_created":"2023-01-23T10:18:48Z","success":1,"file_size":5299475,"content_type":"application/pdf","access_level":"open_access","checksum":"073267a9c0ad9f85a650053bc7b23777","creator":"dernst"}],"oa":1,"citation":{"ieee":"T. Petzold <i>et al.</i>, “Neutrophil ‘plucking’ on megakaryocytes drives platelet production and boosts cardiovascular disease,” <i>Immunity</i>, vol. 55, no. 12. Elsevier, p. 2285–2299.e7, 2022.","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.” <i>Immunity</i>. Elsevier, 2022. <a href=\"https://doi.org/10.1016/j.immuni.2022.10.001\">https://doi.org/10.1016/j.immuni.2022.10.001</a>.","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.","ama":"Petzold T, Zhang Z, Ballesteros I, et al. Neutrophil “plucking” on megakaryocytes drives platelet production and boosts cardiovascular disease. <i>Immunity</i>. 2022;55(12):2285-2299.e7. doi:<a href=\"https://doi.org/10.1016/j.immuni.2022.10.001\">10.1016/j.immuni.2022.10.001</a>","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.","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. <i>Immunity</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.immuni.2022.10.001\">https://doi.org/10.1016/j.immuni.2022.10.001</a>","mla":"Petzold, Tobias, et al. “Neutrophil ‘Plucking’ on Megakaryocytes Drives Platelet Production and Boosts Cardiovascular Disease.” <i>Immunity</i>, vol. 55, no. 12, Elsevier, 2022, p. 2285–2299.e7, doi:<a href=\"https://doi.org/10.1016/j.immuni.2022.10.001\">10.1016/j.immuni.2022.10.001</a>."},"isi":1,"article_type":"original","date_updated":"2025-04-14T07:43:16Z","ddc":["570"]},{"day":"01","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."}],"quality_controlled":"1","fulldoi":"https://doi.org/10.1038/s41577-022-00797-y","issue":"12","publisher":"Springer Nature","doi":"10.1038/s41577-022-00797-y","_id":"12133","keyword":["Energy Engineering and Power Technology","Fuel Technology"],"language":[{"iso":"eng"}],"department":[{"_id":"SyCr"},{"_id":"MiSi"}],"status":"public","page":"713-714","publication":"Nature Reviews Immunology","volume":22,"date_published":"2022-12-01T00:00:00Z","pmid":1,"author":[{"first_name":"Sylvia","orcid":"0000-0002-2193-3868","id":"2F64EC8C-F248-11E8-B48F-1D18A9856A87","full_name":"Cremer, Sylvia","last_name":"Cremer"},{"first_name":"Michael K","orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"}],"publication_status":"published","article_processing_charge":"No","title":"Principles of disease defence in organisms, superorganisms and societies","intvolume":"        22","corr_author":"1","type":"journal_article","publication_identifier":{"issn":["1474-1733"],"eissn":["1474-1741"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","year":"2022","month":"12","external_id":{"isi":["000871836300001"],"pmid":["36284178"]},"oa_version":"None","scopus_import":"1","article_type":"letter_note","isi":1,"date_updated":"2024-10-09T21:03:33Z","citation":{"ieee":"S. Cremer and M. K. Sixt, “Principles of disease defence in organisms, superorganisms and societies,” <i>Nature Reviews Immunology</i>, vol. 22, no. 12. Springer Nature, pp. 713–714, 2022.","chicago":"Cremer, Sylvia, and Michael K Sixt. “Principles of Disease Defence in Organisms, Superorganisms and Societies.” <i>Nature Reviews Immunology</i>. Springer Nature, 2022. <a href=\"https://doi.org/10.1038/s41577-022-00797-y\">https://doi.org/10.1038/s41577-022-00797-y</a>.","ama":"Cremer S, Sixt MK. Principles of disease defence in organisms, superorganisms and societies. <i>Nature Reviews Immunology</i>. 2022;22(12):713-714. doi:<a href=\"https://doi.org/10.1038/s41577-022-00797-y\">10.1038/s41577-022-00797-y</a>","short":"S. Cremer, M.K. Sixt, Nature Reviews Immunology 22 (2022) 713–714.","ista":"Cremer S, Sixt MK. 2022. Principles of disease defence in organisms, superorganisms and societies. Nature Reviews Immunology. 22(12), 713–714.","apa":"Cremer, S., &#38; Sixt, M. K. (2022). Principles of disease defence in organisms, superorganisms and societies. <i>Nature Reviews Immunology</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41577-022-00797-y\">https://doi.org/10.1038/s41577-022-00797-y</a>","mla":"Cremer, Sylvia, and Michael K. Sixt. “Principles of Disease Defence in Organisms, Superorganisms and Societies.” <i>Nature Reviews Immunology</i>, vol. 22, no. 12, Springer Nature, 2022, pp. 713–14, doi:<a href=\"https://doi.org/10.1038/s41577-022-00797-y\">10.1038/s41577-022-00797-y</a>."},"date_created":"2023-01-12T12:03:14Z"},{"status":"public","publication":"Science Advances","article_number":"eabl6293","department":[{"_id":"MiSi"}],"language":[{"iso":"eng"}],"article_processing_charge":"Yes","acknowledgement":"We thank A. L. Horwich, K. Chakraborty, and B. Schuler for providing plasmids, and R. van Leeuwen, M. Mayer, J. van Zon, W. Noorduin, and P. R. ten Wolde for comments and critical reading of the manuscript. Work in the group of S.J.T. was supported by the Netherlands Organization for Scientific Research (NWO). Work in the group of H.S.R. was supported by a grant from the NIH (R01GM114405).","title":"Protein chain collapse modulation and folding stimulation by GroEL-ES","intvolume":"         8","author":[{"first_name":"Mohsin M.","last_name":"Naqvi","full_name":"Naqvi, Mohsin M."},{"last_name":"Avellaneda Sarrió","orcid":"0000-0001-6406-524X","full_name":"Avellaneda Sarrió, Mario","id":"DC4BA84C-56E6-11EA-AD5D-348C3DDC885E","first_name":"Mario"},{"first_name":"Andrew","last_name":"Roth","full_name":"Roth, Andrew"},{"full_name":"Koers, Eline J.","last_name":"Koers","first_name":"Eline J."},{"full_name":"Roland, Antoine","last_name":"Roland","first_name":"Antoine"},{"full_name":"Sunderlikova, Vanda","last_name":"Sunderlikova","first_name":"Vanda"},{"full_name":"Kramer, Günter","last_name":"Kramer","first_name":"Günter"},{"first_name":"Hays S.","full_name":"Rye, Hays S.","last_name":"Rye"},{"last_name":"Tans","full_name":"Tans, Sander J.","first_name":"Sander J."}],"publication_status":"published","volume":8,"pmid":1,"date_published":"2022-03-01T00:00:00Z","issue":"9","fulldoi":"https://doi.org/10.1126/sciadv.abl6293","has_accepted_license":"1","quality_controlled":"1","day":"01","abstract":[{"text":"The collapse of polypeptides is thought important to protein folding, aggregation, intrinsic disorder, and phase separation. However, whether polypeptide collapse is modulated in cells to control protein states is unclear. Here, using integrated protein manipulation and imaging, we show that the chaperonin GroEL-ES can accelerate the folding of proteins by strengthening their collapse. GroEL induces contractile forces in substrate chains, which draws them into the cavity and triggers a general compaction and discrete folding transitions, even for slow-folding proteins. This collapse enhancement is strongest in the nucleotide-bound states of GroEL and is aided by GroES binding to the cavity rim and by the amphiphilic C-terminal tails at the cavity bottom. Collapse modulation is distinct from other proposed GroEL-ES folding acceleration mechanisms, including steric confinement and misfold unfolding. Given the prevalence of collapse throughout the proteome, we conjecture that collapse modulation is more generally relevant within the protein quality control machinery.","lang":"eng"}],"_id":"17072","publisher":"American Association for the Advancement of Science","file_date_updated":"2024-07-31T12:01:51Z","doi":"10.1126/sciadv.abl6293","date_updated":"2024-08-05T08:30:29Z","article_type":"original","ddc":["570"],"date_created":"2024-05-29T06:12:19Z","file":[{"checksum":"9511579306cce7e04107d3d6389ed614","creator":"dernst","success":1,"date_created":"2024-07-31T12:01:51Z","access_level":"open_access","file_size":2404150,"content_type":"application/pdf","relation":"main_file","date_updated":"2024-07-31T12:01:51Z","file_id":"17357","file_name":"2022_ScienceAdv_Naqvi.pdf"}],"citation":{"chicago":"Naqvi, Mohsin M., Mario Avellaneda Sarrió, Andrew Roth, Eline J. Koers, Antoine Roland, Vanda Sunderlikova, Günter Kramer, Hays S. Rye, and Sander J. Tans. “Protein Chain Collapse Modulation and Folding Stimulation by GroEL-ES.” <i>Science Advances</i>. American Association for the Advancement of Science, 2022. <a href=\"https://doi.org/10.1126/sciadv.abl6293\">https://doi.org/10.1126/sciadv.abl6293</a>.","ieee":"M. M. Naqvi <i>et al.</i>, “Protein chain collapse modulation and folding stimulation by GroEL-ES,” <i>Science Advances</i>, vol. 8, no. 9. American Association for the Advancement of Science, 2022.","ista":"Naqvi MM, Avellaneda Sarrió M, Roth A, Koers EJ, Roland A, Sunderlikova V, Kramer G, Rye HS, Tans SJ. 2022. Protein chain collapse modulation and folding stimulation by GroEL-ES. Science Advances. 8(9), eabl6293.","apa":"Naqvi, M. M., Avellaneda Sarrió, M., Roth, A., Koers, E. J., Roland, A., Sunderlikova, V., … Tans, S. J. (2022). Protein chain collapse modulation and folding stimulation by GroEL-ES. <i>Science Advances</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/sciadv.abl6293\">https://doi.org/10.1126/sciadv.abl6293</a>","mla":"Naqvi, Mohsin M., et al. “Protein Chain Collapse Modulation and Folding Stimulation by GroEL-ES.” <i>Science Advances</i>, vol. 8, no. 9, eabl6293, American Association for the Advancement of Science, 2022, doi:<a href=\"https://doi.org/10.1126/sciadv.abl6293\">10.1126/sciadv.abl6293</a>.","ama":"Naqvi MM, Avellaneda Sarrió M, Roth A, et al. Protein chain collapse modulation and folding stimulation by GroEL-ES. <i>Science Advances</i>. 2022;8(9). doi:<a href=\"https://doi.org/10.1126/sciadv.abl6293\">10.1126/sciadv.abl6293</a>","short":"M.M. Naqvi, M. Avellaneda Sarrió, A. Roth, E.J. Koers, A. Roland, V. Sunderlikova, G. Kramer, H.S. Rye, S.J. Tans, Science Advances 8 (2022)."},"oa":1,"year":"2022","publication_identifier":{"issn":["2375-2548"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","type":"journal_article","oa_version":"Published Version","tmp":{"image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)"},"scopus_import":"1","external_id":{"pmid":["35245117"]},"month":"03"},{"intvolume":"        23","title":"Multitier mechanics control stromal adaptations in swelling lymph nodes","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","publication_status":"published","author":[{"first_name":"Frank P","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","full_name":"Assen, Frank P","orcid":"0000-0003-3470-6119","last_name":"Assen"},{"first_name":"Jun","full_name":"Abe, Jun","last_name":"Abe"},{"id":"4167FE56-F248-11E8-B48F-1D18A9856A87","full_name":"Hons, Miroslav","last_name":"Hons","orcid":"0000-0002-6625-3348","first_name":"Miroslav"},{"first_name":"Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9843-3522","last_name":"Hauschild","full_name":"Hauschild, Robert"},{"first_name":"Shayan","last_name":"Shamipour","id":"40B34FE2-F248-11E8-B48F-1D18A9856A87","full_name":"Shamipour, Shayan"},{"first_name":"Walter","full_name":"Kaufmann, Walter","id":"3F99E422-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9735-5315","last_name":"Kaufmann"},{"first_name":"Tommaso","orcid":"0000-0001-9732-3815","id":"D93824F4-D9BA-11E9-BB12-F207E6697425","last_name":"Costanzo","full_name":"Costanzo, Tommaso"},{"first_name":"Gabriel","full_name":"Krens, Gabriel","id":"2B819732-F248-11E8-B48F-1D18A9856A87","last_name":"Krens","orcid":"0000-0003-4761-5996"},{"full_name":"Brown, Markus","id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","last_name":"Brown","first_name":"Markus"},{"first_name":"Burkhard","full_name":"Ludewig, Burkhard","last_name":"Ludewig"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","last_name":"Hippenmeyer","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","first_name":"Simon"},{"orcid":"0000-0002-0912-4566","last_name":"Heisenberg","full_name":"Heisenberg, Carl-Philipp J","id":"39427864-F248-11E8-B48F-1D18A9856A87","first_name":"Carl-Philipp J"},{"first_name":"Wolfgang","last_name":"Weninger","full_name":"Weninger, Wolfgang"},{"full_name":"Hannezo, Edouard B","last_name":"Hannezo","orcid":"0000-0001-6005-1561","id":"3A9DB764-F248-11E8-B48F-1D18A9856A87","first_name":"Edouard B"},{"full_name":"Luther, Sanjiv A.","last_name":"Luther","first_name":"Sanjiv A."},{"first_name":"Jens V.","full_name":"Stein, Jens V.","last_name":"Stein"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","orcid":"0000-0002-4561-241X","last_name":"Sixt","first_name":"Michael K"}],"acknowledged_ssus":[{"_id":"Bio"},{"_id":"EM-Fac"},{"_id":"PreCl"},{"_id":"LifeSc"}],"volume":23,"date_published":"2022-07-11T00:00:00Z","pmid":1,"publication":"Nature Immunology","status":"public","page":"1246-1255","ec_funded":1,"department":[{"_id":"SiHi"},{"_id":"CaHe"},{"_id":"EdHa"},{"_id":"EM-Fac"},{"_id":"Bio"},{"_id":"MiSi"}],"language":[{"iso":"eng"}],"_id":"9794","doi":"10.1038/s41590-022-01257-4","file_date_updated":"2022-07-25T07:11:32Z","publisher":"Springer Nature","fulldoi":"https://doi.org/10.1038/s41590-022-01257-4","has_accepted_license":"1","quality_controlled":"1","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."}],"day":"11","file":[{"creator":"dernst","checksum":"628e7b49809f22c75b428842efe70c68","access_level":"open_access","content_type":"application/pdf","file_size":11475325,"success":1,"date_created":"2022-07-25T07:11:32Z","relation":"main_file","file_name":"2022_NatureImmunology_Assen.pdf","date_updated":"2022-07-25T07:11:32Z","file_id":"11642"}],"date_created":"2021-08-06T09:09:11Z","oa":1,"citation":{"mla":"Assen, Frank P., et al. “Multitier Mechanics Control Stromal Adaptations in Swelling Lymph Nodes.” <i>Nature Immunology</i>, vol. 23, Springer Nature, 2022, pp. 1246–55, doi:<a href=\"https://doi.org/10.1038/s41590-022-01257-4\">10.1038/s41590-022-01257-4</a>.","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. <i>Nature Immunology</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41590-022-01257-4\">https://doi.org/10.1038/s41590-022-01257-4</a>","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.","ama":"Assen FP, Abe J, Hons M, et al. Multitier mechanics control stromal adaptations in swelling lymph nodes. <i>Nature Immunology</i>. 2022;23:1246-1255. doi:<a href=\"https://doi.org/10.1038/s41590-022-01257-4\">10.1038/s41590-022-01257-4</a>","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.","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.” <i>Nature Immunology</i>. Springer Nature, 2022. <a href=\"https://doi.org/10.1038/s41590-022-01257-4\">https://doi.org/10.1038/s41590-022-01257-4</a>.","ieee":"F. P. Assen <i>et al.</i>, “Multitier mechanics control stromal adaptations in swelling lymph nodes,” <i>Nature Immunology</i>, vol. 23. Springer Nature, pp. 1246–1255, 2022."},"date_updated":"2025-06-11T13:52:43Z","isi":1,"article_type":"original","ddc":["570"],"tmp":{"image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)"},"scopus_import":"1","oa_version":"Published Version","external_id":{"isi":["000822975900002"],"pmid":["35817845"]},"month":"07","year":"2022","project":[{"call_identifier":"H2020","grant_number":"724373","name":"Cellular Navigation Along Spatial Gradients","_id":"25FE9508-B435-11E9-9278-68D0E5697425"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"issn":["1529-2908"],"eissn":["1529-2916"]},"type":"journal_article","corr_author":"1"},{"quality_controlled":"1","abstract":[{"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.","lang":"eng"}],"day":"26","has_accepted_license":"1","fulldoi":"https://doi.org/10.7554/eLife.78995","doi":"10.7554/eLife.78995","file_date_updated":"2022-08-16T08:57:37Z","publisher":"eLife Sciences Publications","_id":"11843","related_material":{"record":[{"status":"public","id":"10316","relation":"earlier_version"}]},"language":[{"iso":"eng"}],"publication":"eLife","article_number":"e78995","status":"public","ec_funded":1,"department":[{"_id":"MiSi"},{"_id":"CaGu"}],"acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"},{"_id":"EM-Fac"}],"date_published":"2022-07-26T00:00:00Z","pmid":1,"volume":11,"title":"Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14","intvolume":"        11","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_processing_charge":"Yes","publication_status":"published","author":[{"first_name":"Kathrin","last_name":"Tomasek","id":"3AEC8556-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-3768-877X","full_name":"Tomasek, Kathrin"},{"orcid":"0000-0002-1073-744X","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","full_name":"Leithner, Alexander F","last_name":"Leithner","first_name":"Alexander F"},{"first_name":"Ivana","full_name":"Glatzová, Ivana","last_name":"Glatzová","id":"727b3c7d-4939-11ec-89b3-b9b0750ab74d"},{"last_name":"Lukesch","full_name":"Lukesch, Michael S.","first_name":"Michael S."},{"last_name":"Guet","full_name":"Guet, Calin C","id":"47F8433E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6220-2052","first_name":"Calin C"},{"orcid":"0000-0002-6620-9179","full_name":"Sixt, Michael K","last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}],"publication_identifier":{"eissn":["2050-084X"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","corr_author":"1","type":"journal_article","project":[{"call_identifier":"H2020","name":"Cellular Navigation Along Spatial Gradients","grant_number":"724373","_id":"25FE9508-B435-11E9-9278-68D0E5697425"},{"_id":"26018E70-B435-11E9-9278-68D0E5697425","grant_number":"P29911","name":"Mechanical adaptation of lamellipodial actin","call_identifier":"FWF"}],"year":"2022","external_id":{"pmid":["35881547"],"isi":["000838410200001"]},"month":"07","scopus_import":"1","tmp":{"image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)"},"oa_version":"Published Version","ddc":["570"],"date_updated":"2026-07-06T12:48:19Z","article_type":"original","isi":1,"oa":1,"citation":{"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.","apa":"Tomasek, K., Leithner, A. F., Glatzová, I., Lukesch, M. S., Guet, C. C., &#38; Sixt, M. K. (2022). Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/eLife.78995\">https://doi.org/10.7554/eLife.78995</a>","mla":"Tomasek, Kathrin, et al. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack the Host Immune Response by Binding to CD14.” <i>ELife</i>, vol. 11, e78995, eLife Sciences Publications, 2022, doi:<a href=\"https://doi.org/10.7554/eLife.78995\">10.7554/eLife.78995</a>.","short":"K. Tomasek, A.F. Leithner, I. Glatzová, M.S. Lukesch, C.C. Guet, M.K. Sixt, ELife 11 (2022).","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. <i>eLife</i>. 2022;11. doi:<a href=\"https://doi.org/10.7554/eLife.78995\">10.7554/eLife.78995</a>","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.” <i>ELife</i>. eLife Sciences Publications, 2022. <a href=\"https://doi.org/10.7554/eLife.78995\">https://doi.org/10.7554/eLife.78995</a>.","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,” <i>eLife</i>, vol. 11. eLife Sciences Publications, 2022."},"file":[{"relation":"main_file","date_updated":"2022-08-16T08:57:37Z","file_id":"11861","file_name":"2022_eLife_Tomasek.pdf","checksum":"002a3c7c7ea5caa9af9cfbea308f6ea4","creator":"cchlebak","date_created":"2022-08-16T08:57:37Z","success":1,"content_type":"application/pdf","file_size":2057577,"access_level":"open_access"}],"date_created":"2022-08-14T22:01:46Z"},{"type":"journal_article","corr_author":"1","publication_identifier":{"eissn":["1878-1551"],"issn":["1534-5807"]},"user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","project":[{"_id":"260AA4E2-B435-11E9-9278-68D0E5697425","grant_number":"747687","name":"Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells","call_identifier":"H2020"},{"_id":"25FE9508-B435-11E9-9278-68D0E5697425","name":"Cellular Navigation Along Spatial Gradients","grant_number":"724373","call_identifier":"H2020"}],"year":"2022","month":"01","external_id":{"pmid":["34919802"],"isi":["000768933800005"]},"oa_version":"Published Version","scopus_import":"1","tmp":{"image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)"},"main_file_link":[{"open_access":"1","url":"https://www.sciencedirect.com/science/article/pii/S1534580721009497"}],"ddc":["570"],"isi":1,"article_type":"original","date_updated":"2026-09-28T22:30:13Z","citation":{"short":"F. Gaertner, P. Dos 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.","ama":"Gaertner F, Dos Reis Rodrigues P, de Vries I, et al. WASp triggers mechanosensitive actin patches to facilitate immune cell migration in dense tissues. <i>Developmental Cell</i>. 2022;57(1):47-62.e9. doi:<a href=\"https://doi.org/10.1016/j.devcel.2021.11.024\">10.1016/j.devcel.2021.11.024</a>","ista":"Gaertner F, Dos 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.","apa":"Gaertner, F., Dos 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. <i>Developmental Cell</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.devcel.2021.11.024\">https://doi.org/10.1016/j.devcel.2021.11.024</a>","mla":"Gaertner, Florian, et al. “WASp Triggers Mechanosensitive Actin Patches to Facilitate Immune Cell Migration in Dense Tissues.” <i>Developmental Cell</i>, vol. 57, no. 1, Cell Press, 2022, p. 47–62.e9, doi:<a href=\"https://doi.org/10.1016/j.devcel.2021.11.024\">10.1016/j.devcel.2021.11.024</a>.","ieee":"F. Gaertner <i>et al.</i>, “WASp triggers mechanosensitive actin patches to facilitate immune cell migration in dense tissues,” <i>Developmental Cell</i>, vol. 57, no. 1. Cell Press, p. 47–62.e9, 2022.","chicago":"Gaertner, Florian, Patricia Dos 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.” <i>Developmental Cell</i>. Cell Press, 2022. <a href=\"https://doi.org/10.1016/j.devcel.2021.11.024\">https://doi.org/10.1016/j.devcel.2021.11.024</a>."},"oa":1,"date_created":"2022-01-30T23:01:33Z","day":"10","abstract":[{"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.","lang":"eng"}],"quality_controlled":"1","fulldoi":"https://doi.org/10.1016/j.devcel.2021.11.024","issue":"1","publisher":"Cell Press","doi":"10.1016/j.devcel.2021.11.024","_id":"10703","language":[{"iso":"eng"}],"related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"20149"},{"relation":"dissertation_contains","id":"12726","status":"public"},{"status":"public","relation":"dissertation_contains","id":"14530"},{"relation":"dissertation_contains","id":"12401","status":"public"}]},"department":[{"_id":"MiSi"},{"_id":"EM-Fac"},{"_id":"NanoFab"},{"_id":"BjHo"}],"ec_funded":1,"status":"public","page":"47-62.e9","publication":"Developmental Cell","volume":57,"pmid":1,"date_published":"2022-01-10T00:00:00Z","acknowledged_ssus":[{"_id":"LifeSc"},{"_id":"Bio"},{"_id":"EM-Fac"}],"publication_status":"published","author":[{"first_name":"Florian","last_name":"Gaertner","full_name":"Gaertner, Florian"},{"orcid":"0000-0003-1681-508X","id":"26E95904-5160-11E9-9C0B-C5B0DC97E90F","full_name":"Dos Reis Rodrigues, Patricia","last_name":"Dos Reis Rodrigues","first_name":"Patricia"},{"first_name":"Ingrid","id":"4C7D837E-F248-11E8-B48F-1D18A9856A87","last_name":"De Vries","full_name":"De Vries, Ingrid"},{"last_name":"Hons","id":"4167FE56-F248-11E8-B48F-1D18A9856A87","full_name":"Hons, Miroslav","orcid":"0000-0002-6625-3348","first_name":"Miroslav"},{"last_name":"Aguilera","full_name":"Aguilera, Juan","first_name":"Juan"},{"first_name":"Michael","orcid":"0000-0003-4844-6311","full_name":"Riedl, Michael","last_name":"Riedl","id":"3BE60946-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Alexander F","full_name":"Leithner, Alexander F","orcid":"0000-0002-1073-744X","last_name":"Leithner","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Saren","full_name":"Tasciyan, Saren","orcid":"0000-0003-1671-393X","last_name":"Tasciyan","id":"4323B49C-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Aglaja","full_name":"Kopf, Aglaja","last_name":"Kopf","orcid":"0000-0002-2187-6656","id":"31DAC7B6-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Jack","last_name":"Merrin","full_name":"Merrin, Jack","id":"4515C308-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5145-4609"},{"first_name":"Vanessa","last_name":"Zheden","id":"39C5A68A-F248-11E8-B48F-1D18A9856A87","full_name":"Zheden, Vanessa","orcid":"0000-0002-9438-4783"},{"last_name":"Kaufmann","id":"3F99E422-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9735-5315","full_name":"Kaufmann, Walter","first_name":"Walter"},{"last_name":"Hauschild","full_name":"Hauschild, Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-9843-3522","first_name":"Robert"},{"full_name":"Sixt, Michael K","last_name":"Sixt","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"}],"article_processing_charge":"No","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.","title":"WASp triggers mechanosensitive actin patches to facilitate immune cell migration in dense tissues","intvolume":"        57"},{"_id":"12401","OA_place":"publisher","doi":"10.15479/at:ista:12401","file_date_updated":"2023-12-21T23:30:03Z","publisher":"Institute of Science and Technology Austria","degree_awarded":"PhD","fulldoi":"https://doi.org/10.15479/at:ista:12401","has_accepted_license":"1","abstract":[{"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.","lang":"eng"}],"day":"22","publication_status":"published","author":[{"first_name":"Saren","id":"4323B49C-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-1671-393X","full_name":"Tasciyan, Saren","last_name":"Tasciyan"}],"title":"Role of microenvironment heterogeneity in cancer cell invasion","article_processing_charge":"No","date_published":"2022-12-22T00:00:00Z","department":[{"_id":"GradSch"},{"_id":"MiSi"}],"page":"105","status":"public","related_material":{"record":[{"status":"public","id":"7885","relation":"part_of_dissertation"},{"status":"public","relation":"part_of_dissertation","id":"10703"},{"relation":"part_of_dissertation","id":"679","status":"public"},{"status":"public","id":"9429","relation":"part_of_dissertation"}]},"language":[{"iso":"eng"}],"oa_version":"Published Version","alternative_title":["ISTA Thesis"],"month":"12","year":"2022","corr_author":"1","type":"dissertation","user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","publication_identifier":{"issn":["2663-337X"]},"date_created":"2023-01-26T11:55:16Z","file":[{"relation":"main_file","embargo":"2023-12-20","file_name":"PhD-Thesis_Saren Tasciyan_formatted_aftercrash_fixed_600dpi_95pc_final_PDFA3b.pdf","file_id":"12402","date_updated":"2023-12-21T23:30:03Z","creator":"cchlebak","checksum":"cc4a2b4a7e3c4ee8ef7f2dbf909b12bd","content_type":"application/pdf","file_size":42059787,"access_level":"open_access","date_created":"2023-01-26T11:58:14Z"},{"relation":"source_file","file_name":"Source Files - Saren Tasciyan - PhD Thesis.zip","file_id":"12403","date_updated":"2023-12-21T23:30:03Z","creator":"cchlebak","embargo_to":"open_access","checksum":"f1b4ca98b8ab0cb043b1830971e9bd9c","access_level":"closed","content_type":"application/x-zip-compressed","file_size":261256696,"date_created":"2023-01-26T12:00:10Z"}],"oa":1,"citation":{"apa":"Tasciyan, S. (2022). <i>Role of microenvironment heterogeneity in cancer cell invasion</i>. Institute of Science and Technology Austria. <a href=\"https://doi.org/10.15479/at:ista:12401\">https://doi.org/10.15479/at:ista:12401</a>","mla":"Tasciyan, Saren. <i>Role of Microenvironment Heterogeneity in Cancer Cell Invasion</i>. Institute of Science and Technology Austria, 2022, doi:<a href=\"https://doi.org/10.15479/at:ista:12401\">10.15479/at:ista:12401</a>.","ista":"Tasciyan S. 2022. Role of microenvironment heterogeneity in cancer cell invasion. Institute of Science and Technology Austria.","short":"S. Tasciyan, Role of Microenvironment Heterogeneity in Cancer Cell Invasion, Institute of Science and Technology Austria, 2022.","ama":"Tasciyan S. Role of microenvironment heterogeneity in cancer cell invasion. 2022. doi:<a href=\"https://doi.org/10.15479/at:ista:12401\">10.15479/at:ista:12401</a>","chicago":"Tasciyan, Saren. “Role of Microenvironment Heterogeneity in Cancer Cell Invasion.” Institute of Science and Technology Austria, 2022. <a href=\"https://doi.org/10.15479/at:ista:12401\">https://doi.org/10.15479/at:ista:12401</a>.","ieee":"S. Tasciyan, “Role of microenvironment heterogeneity in cancer cell invasion,” Institute of Science and Technology Austria, 2022."},"supervisor":[{"orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","full_name":"Sixt, Michael K","first_name":"Michael K"}],"date_updated":"2026-04-14T09:07:14Z","ddc":["610"]},{"article_type":"original","isi":1,"date_updated":"2026-09-28T22:30:17Z","ddc":["570"],"date_created":"2023-01-16T10:01:08Z","file":[{"access_level":"open_access","file_size":969969,"content_type":"application/pdf","success":1,"date_created":"2023-01-30T10:39:34Z","creator":"dernst","checksum":"6b1620743669679b48b9389bb40f5a11","file_name":"2022_JourCellBiology_Stopp.pdf","file_id":"12451","date_updated":"2023-01-30T10:39:34Z","relation":"main_file"}],"citation":{"ama":"Stopp JA, Sixt MK. Plan your trip before you leave: The neutrophils’ search-and-run journey. <i>Journal of Cell Biology</i>. 2022;221(8). doi:<a href=\"https://doi.org/10.1083/jcb.202206127\">10.1083/jcb.202206127</a>","short":"J.A. Stopp, M.K. Sixt, Journal of Cell Biology 221 (2022).","mla":"Stopp, Julian A., and Michael K. Sixt. “Plan Your Trip before You Leave: The Neutrophils’ Search-and-Run Journey.” <i>Journal of Cell Biology</i>, vol. 221, no. 8, e202206127, Rockefeller University Press, 2022, doi:<a href=\"https://doi.org/10.1083/jcb.202206127\">10.1083/jcb.202206127</a>.","apa":"Stopp, J. A., &#38; Sixt, M. K. (2022). Plan your trip before you leave: The neutrophils’ search-and-run journey. <i>Journal of Cell Biology</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1083/jcb.202206127\">https://doi.org/10.1083/jcb.202206127</a>","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.","ieee":"J. A. Stopp and M. K. Sixt, “Plan your trip before you leave: The neutrophils’ search-and-run journey,” <i>Journal of Cell Biology</i>, vol. 221, no. 8. Rockefeller University Press, 2022.","chicago":"Stopp, Julian A, and Michael K Sixt. “Plan Your Trip before You Leave: The Neutrophils’ Search-and-Run Journey.” <i>Journal of Cell Biology</i>. Rockefeller University Press, 2022. <a href=\"https://doi.org/10.1083/jcb.202206127\">https://doi.org/10.1083/jcb.202206127</a>."},"oa":1,"year":"2022","corr_author":"1","type":"journal_article","publication_identifier":{"eissn":["1540-8140"],"issn":["0021-9525"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","oa_version":"Published Version","tmp":{"name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","image":"/images/cc_by_nc_sa.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","short":"CC BY-NC-SA (4.0)"},"scopus_import":"1","month":"07","external_id":{"pmid":["35856919"],"isi":["000874717200001"]},"department":[{"_id":"MiSi"}],"status":"public","article_number":"e202206127","publication":"Journal of Cell Biology","language":[{"iso":"eng"}],"related_material":{"record":[{"status":"public","id":"14697","relation":"dissertation_contains"}]},"author":[{"first_name":"Julian A","full_name":"Stopp, Julian A","last_name":"Stopp","id":"489E3F00-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt","full_name":"Sixt, Michael K"}],"publication_status":"published","article_processing_charge":"No","title":"Plan your trip before you leave: The neutrophils’ search-and-run journey","intvolume":"       221","volume":221,"pmid":1,"date_published":"2022-07-20T00:00:00Z","issue":"8","fulldoi":"https://doi.org/10.1083/jcb.202206127","has_accepted_license":"1","day":"20","abstract":[{"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.","lang":"eng"}],"quality_controlled":"1","_id":"12272","license":"https://creativecommons.org/licenses/by-nc-sa/4.0/","keyword":["Cell Biology"],"publisher":"Rockefeller University Press","file_date_updated":"2023-01-30T10:39:34Z","doi":"10.1083/jcb.202206127"},{"publication_identifier":{"issn":["0960-9822"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","type":"journal_article","year":"2021","external_id":{"isi":["000654652200002"],"pmid":["33711252"]},"month":"05","main_file_link":[{"url":"https://doi.org/10.1101/2020.03.24.005835","open_access":"1"}],"oa_version":"Preprint","scopus_import":"1","date_updated":"2023-08-17T07:01:14Z","article_type":"original","isi":1,"citation":{"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.","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. <i>Current Biology</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.cub.2021.02.043\">https://doi.org/10.1016/j.cub.2021.02.043</a>","mla":"Stahnke, Stephanie, et al. “Loss of Hem1 Disrupts Macrophage Function and Impacts Migration, Phagocytosis, and Integrin-Mediated Adhesion.” <i>Current Biology</i>, vol. 31, no. 10, Elsevier, 2021, p. 2051–2064.e8, doi:<a href=\"https://doi.org/10.1016/j.cub.2021.02.043\">10.1016/j.cub.2021.02.043</a>.","ama":"Stahnke S, Döring H, Kusch C, et al. Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis, and integrin-mediated adhesion. <i>Current Biology</i>. 2021;31(10):2051-2064.e8. doi:<a href=\"https://doi.org/10.1016/j.cub.2021.02.043\">10.1016/j.cub.2021.02.043</a>","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.","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.” <i>Current Biology</i>. Elsevier, 2021. <a href=\"https://doi.org/10.1016/j.cub.2021.02.043\">https://doi.org/10.1016/j.cub.2021.02.043</a>.","ieee":"S. Stahnke <i>et al.</i>, “Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis, and integrin-mediated adhesion,” <i>Current Biology</i>, vol. 31, no. 10. Elsevier, p. 2051–2064.e8, 2021."},"oa":1,"date_created":"2022-03-08T07:51:04Z","quality_controlled":"1","day":"24","abstract":[{"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.","lang":"eng"}],"fulldoi":"https://doi.org/10.1016/j.cub.2021.02.043","issue":"10","publisher":"Elsevier","doi":"10.1016/j.cub.2021.02.043","keyword":["General Agricultural and Biological Sciences","General Biochemistry","Genetics and Molecular Biology"],"_id":"10834","language":[{"iso":"eng"}],"status":"public","page":"2051-2064.e8","publication":"Current Biology","department":[{"_id":"MiSi"}],"date_published":"2021-05-24T00:00:00Z","pmid":1,"volume":31,"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","title":"Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis, and integrin-mediated adhesion","intvolume":"        31","author":[{"first_name":"Stephanie","last_name":"Stahnke","full_name":"Stahnke, Stephanie"},{"full_name":"Döring, Hermann","last_name":"Döring","first_name":"Hermann"},{"last_name":"Kusch","full_name":"Kusch, Charly","first_name":"Charly"},{"first_name":"David J.J.","last_name":"de Gorter","full_name":"de Gorter, David J.J."},{"first_name":"Sebastian","last_name":"Dütting","full_name":"Dütting, Sebastian"},{"first_name":"Aleks","last_name":"Guledani","full_name":"Guledani, Aleks"},{"first_name":"Irina","last_name":"Pleines","full_name":"Pleines, Irina"},{"last_name":"Schnoor","full_name":"Schnoor, Michael","first_name":"Michael"},{"id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","last_name":"Sixt","orcid":"0000-0002-6620-9179","first_name":"Michael K"},{"first_name":"Robert","last_name":"Geffers","full_name":"Geffers, Robert"},{"last_name":"Rohde","full_name":"Rohde, Manfred","first_name":"Manfred"},{"first_name":"Mathias","last_name":"Müsken","full_name":"Müsken, Mathias"},{"last_name":"Kage","full_name":"Kage, Frieda","first_name":"Frieda"},{"first_name":"Anika","full_name":"Steffen, Anika","last_name":"Steffen"},{"full_name":"Faix, Jan","last_name":"Faix","first_name":"Jan"},{"last_name":"Nieswandt","full_name":"Nieswandt, Bernhard","first_name":"Bernhard"},{"first_name":"Klemens","last_name":"Rottner","full_name":"Rottner, Klemens"},{"first_name":"Theresia E.B.","last_name":"Stradal","full_name":"Stradal, Theresia E.B."}],"publication_status":"published"},{"date_created":"2021-01-03T23:01:23Z","oa":1,"citation":{"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.” <i>Proceedings of the National Academy of Sciences of the United States of America</i>. National Academy of Sciences, 2021. <a href=\"https://doi.org/10.1073/pnas.2010054118\">https://doi.org/10.1073/pnas.2010054118</a>.","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,” <i>Proceedings of the National Academy of Sciences of the United States of America</i>, 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. Proceedings of the National Academy of Sciences of the United States of America. 118(1), e2010054118.","apa":"Düllberg, C. F., Auer, A., Canigova, N., Loibl, K., &#38; Loose, M. (2021). In vitro reconstitution reveals phosphoinositides as cargo-release factors and activators of the ARF6 GAP ADAP1. <i>Proceedings of the National Academy of Sciences of the United States of America</i>. National Academy of Sciences. <a href=\"https://doi.org/10.1073/pnas.2010054118\">https://doi.org/10.1073/pnas.2010054118</a>","mla":"Düllberg, Christian F., et al. “In Vitro Reconstitution Reveals Phosphoinositides as Cargo-Release Factors and Activators of the ARF6 GAP ADAP1.” <i>Proceedings of the National Academy of Sciences of the United States of America</i>, vol. 118, no. 1, e2010054118, National Academy of Sciences, 2021, doi:<a href=\"https://doi.org/10.1073/pnas.2010054118\">10.1073/pnas.2010054118</a>.","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. <i>Proceedings of the National Academy of Sciences of the United States of America</i>. 2021;118(1). doi:<a href=\"https://doi.org/10.1073/pnas.2010054118\">10.1073/pnas.2010054118</a>","short":"C.F. Düllberg, A. Auer, N. Canigova, K. Loibl, M. Loose, Proceedings of the National Academy of Sciences of the United States of America 118 (2021)."},"article_type":"original","isi":1,"date_updated":"2026-06-18T19:37:53Z","ddc":["570"],"scopus_import":"1","oa_version":"Published Version","main_file_link":[{"open_access":"1","url":"https://doi.org/10.1073/pnas.2010054118"}],"month":"01","external_id":{"isi":["000607270100018"],"pmid":["33443153"]},"project":[{"grant_number":"RGY0083/2016","name":"Reconstitution of cell polarity and axis determination in a cell-free system","_id":"2599F062-B435-11E9-9278-68D0E5697425"}],"year":"2021","type":"journal_article","corr_author":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"issn":["0027-8424"],"eissn":["1091-6490"]},"author":[{"last_name":"Düllberg","orcid":"0000-0001-6335-9748","id":"459064DC-F248-11E8-B48F-1D18A9856A87","full_name":"Düllberg, Christian F","first_name":"Christian F"},{"first_name":"Albert","full_name":"Auer, Albert","id":"3018E8C2-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-3580-2906","last_name":"Auer"},{"first_name":"Nikola","id":"3795523E-F248-11E8-B48F-1D18A9856A87","last_name":"Canigova","orcid":"0000-0002-8518-5926","full_name":"Canigova, Nikola"},{"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","orcid":"0000-0001-7309-9724","last_name":"Loose","id":"462D4284-F248-11E8-B48F-1D18A9856A87"}],"publication_status":"published","intvolume":"       118","title":"In vitro reconstitution reveals phosphoinositides as cargo-release factors and activators of the ARF6 GAP ADAP1","article_processing_charge":"No","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. ","volume":118,"date_published":"2021-01-05T00:00:00Z","pmid":1,"acknowledged_ssus":[{"_id":"Bio"},{"_id":"LifeSc"},{"_id":"EM-Fac"}],"department":[{"_id":"MaLo"},{"_id":"MiSi"}],"publication":"Proceedings of the National Academy of Sciences of the United States of America","article_number":"e2010054118","status":"public","language":[{"iso":"eng"}],"_id":"8988","doi":"10.1073/pnas.2010054118","publisher":"National Academy of Sciences","fulldoi":"https://doi.org/10.1073/pnas.2010054118","issue":"1","abstract":[{"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.","lang":"eng"}],"day":"05","quality_controlled":"1"},{"quality_controlled":"1","abstract":[{"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.","lang":"eng"}],"day":"05","issue":"4","fulldoi":"https://doi.org/10.1083/jcb.202006081","has_accepted_license":"1","doi":"10.1083/jcb.202006081","file_date_updated":"2022-05-12T14:16:21Z","publisher":"Rockefeller University Press","_id":"9094","language":[{"iso":"eng"}],"article_number":"e202006081","publication":"Journal of Cell Biology","status":"public","department":[{"_id":"MiSi"}],"pmid":1,"volume":220,"date_published":"2021-04-05T00:00:00Z","intvolume":"       220","title":"Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse","article_processing_charge":"No","publication_status":"published","author":[{"first_name":"Alexander F","last_name":"Leithner","id":"3B1B77E4-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-1073-744X","full_name":"Leithner, Alexander F"},{"full_name":"Altenburger, LM","last_name":"Altenburger","first_name":"LM"},{"first_name":"R","full_name":"Hauschild, R","last_name":"Hauschild"},{"full_name":"Assen, Frank P","id":"3A8E7F24-F248-11E8-B48F-1D18A9856A87","last_name":"Assen","orcid":"0000-0003-3470-6119","first_name":"Frank P"},{"first_name":"K","full_name":"Rottner, K","last_name":"Rottner"},{"full_name":"TEB, Stradal","last_name":"TEB","first_name":"Stradal"},{"last_name":"Diz-Muñoz","full_name":"Diz-Muñoz, A","first_name":"A"},{"first_name":"JV","last_name":"Stein","full_name":"Stein, JV"},{"last_name":"Sixt","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","first_name":"Michael K"}],"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","publication_identifier":{"issn":["0021-9525"],"eissn":["1540-8140"]},"corr_author":"1","type":"journal_article","year":"2021","external_id":{"pmid":["33533935"],"isi":["000626365700001"]},"month":"04","scopus_import":"1","tmp":{"name":"Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)","image":"/images/cc_by_nc_sa.png","legal_code_url":"https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode","short":"CC BY-NC-SA (4.0)"},"oa_version":"Published Version","ddc":["570"],"date_updated":"2024-10-09T21:00:23Z","isi":1,"article_type":"original","oa":1,"citation":{"ieee":"A. F. Leithner <i>et al.</i>, “Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse,” <i>Journal of Cell Biology</i>, vol. 220, no. 4. Rockefeller University Press, 2021.","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.” <i>Journal of Cell Biology</i>. Rockefeller University Press, 2021. <a href=\"https://doi.org/10.1083/jcb.202006081\">https://doi.org/10.1083/jcb.202006081</a>.","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).","ama":"Leithner AF, Altenburger L, Hauschild R, et al. Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse. <i>Journal of Cell Biology</i>. 2021;220(4). doi:<a href=\"https://doi.org/10.1083/jcb.202006081\">10.1083/jcb.202006081</a>","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.” <i>Journal of Cell Biology</i>, vol. 220, no. 4, e202006081, Rockefeller University Press, 2021, doi:<a href=\"https://doi.org/10.1083/jcb.202006081\">10.1083/jcb.202006081</a>.","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. <i>Journal of Cell Biology</i>. Rockefeller University Press. <a href=\"https://doi.org/10.1083/jcb.202006081\">https://doi.org/10.1083/jcb.202006081</a>"},"date_created":"2021-02-05T10:08:04Z","file":[{"creator":"dernst","checksum":"843ebc153847c8626e13c9c5ce71d533","file_size":5102328,"content_type":"application/pdf","access_level":"open_access","date_created":"2022-05-12T14:16:21Z","success":1,"relation":"main_file","file_name":"2021_JournCellBiology_Leithner.pdf","file_id":"11367","date_updated":"2022-05-12T14:16:21Z"}]},{"file":[{"file_name":"2021_FrontiersImmumo_Vaahtomeri.pdf","date_updated":"2021-03-22T12:08:26Z","file_id":"9277","relation":"main_file","file_size":3740146,"content_type":"application/pdf","access_level":"open_access","date_created":"2021-03-22T12:08:26Z","success":1,"creator":"dernst","checksum":"663f5a48375e42afa4bfef58d42ec186"}],"date_created":"2021-03-21T23:01:20Z","oa":1,"citation":{"apa":"Vaahtomeri, K., Moussion, C., Hauschild, R., &#38; Sixt, M. K. (2021). Shape and function of interstitial chemokine CCL21 gradients are independent of heparan sulfates produced by lymphatic endothelium. <i>Frontiers in Immunology</i>. Frontiers. <a href=\"https://doi.org/10.3389/fimmu.2021.630002\">https://doi.org/10.3389/fimmu.2021.630002</a>","mla":"Vaahtomeri, Kari, et al. “Shape and Function of Interstitial Chemokine CCL21 Gradients Are Independent of Heparan Sulfates Produced by Lymphatic Endothelium.” <i>Frontiers in Immunology</i>, vol. 12, 630002, Frontiers, 2021, doi:<a href=\"https://doi.org/10.3389/fimmu.2021.630002\">10.3389/fimmu.2021.630002</a>.","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.","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. <i>Frontiers in Immunology</i>. 2021;12. doi:<a href=\"https://doi.org/10.3389/fimmu.2021.630002\">10.3389/fimmu.2021.630002</a>","short":"K. Vaahtomeri, C. Moussion, R. Hauschild, M.K. Sixt, Frontiers in Immunology 12 (2021).","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.” <i>Frontiers in Immunology</i>. Frontiers, 2021. <a href=\"https://doi.org/10.3389/fimmu.2021.630002\">https://doi.org/10.3389/fimmu.2021.630002</a>.","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,” <i>Frontiers in Immunology</i>, vol. 12. Frontiers, 2021."},"article_type":"original","isi":1,"date_updated":"2025-04-14T07:42:07Z","ddc":["570"],"tmp":{"image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)"},"scopus_import":"1","oa_version":"Published Version","month":"02","external_id":{"pmid":["33717158"],"isi":["000627134400001"]},"year":"2021","project":[{"_id":"25FE9508-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","name":"Cellular Navigation Along Spatial Gradients","grant_number":"724373"},{"_id":"25A8E5EA-B435-11E9-9278-68D0E5697425","name":"Cytoskeletal force generation and force transduction of migrating leukocytes","grant_number":"Y 564-B12","call_identifier":"FWF"}],"corr_author":"1","type":"journal_article","publication_identifier":{"eissn":["1664-3224"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","publication_status":"published","author":[{"first_name":"Kari","orcid":"0000-0001-7829-3518","last_name":"Vaahtomeri","id":"368EE576-F248-11E8-B48F-1D18A9856A87","full_name":"Vaahtomeri, Kari"},{"id":"3356F664-F248-11E8-B48F-1D18A9856A87","full_name":"Moussion, Christine","last_name":"Moussion","first_name":"Christine"},{"first_name":"Robert","last_name":"Hauschild","orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","full_name":"Hauschild, Robert"},{"last_name":"Sixt","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","first_name":"Michael K"}],"intvolume":"        12","title":"Shape and function of interstitial chemokine CCL21 gradients are independent of heparan sulfates produced by lymphatic endothelium","article_processing_charge":"No","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.","date_published":"2021-02-25T00:00:00Z","pmid":1,"volume":12,"ec_funded":1,"department":[{"_id":"MiSi"},{"_id":"Bio"}],"article_number":"630002","publication":"Frontiers in Immunology","status":"public","language":[{"iso":"eng"}],"_id":"9259","file_date_updated":"2021-03-22T12:08:26Z","doi":"10.3389/fimmu.2021.630002","publisher":"Frontiers","has_accepted_license":"1","fulldoi":"https://doi.org/10.3389/fimmu.2021.630002","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."}],"day":"25","quality_controlled":"1"},{"year":"2021","type":"journal_article","corr_author":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"issn":["1534-5807"],"eissn":["1878-1551"]},"scopus_import":"1","oa_version":"Published Version","main_file_link":[{"url":"https://doi.org/10.1016/j.devcel.2021.03.002","open_access":"1"}],"month":"03","external_id":{"pmid":["33756118"],"isi":["000631681200004"]},"isi":1,"article_type":"original","date_updated":"2026-06-18T19:45:10Z","ddc":["570"],"date_created":"2021-03-28T22:01:41Z","oa":1,"citation":{"ieee":"F. R. Gärtner and M. K. Sixt, “Engaging the front wheels to drive through fibrous terrain,” <i>Developmental Cell</i>, vol. 56, no. 6. Elsevier, pp. 723–725, 2021.","chicago":"Gärtner, Florian R, and Michael K Sixt. “Engaging the Front Wheels to Drive through Fibrous Terrain.” <i>Developmental Cell</i>. Elsevier, 2021. <a href=\"https://doi.org/10.1016/j.devcel.2021.03.002\">https://doi.org/10.1016/j.devcel.2021.03.002</a>.","short":"F.R. Gärtner, M.K. Sixt, Developmental Cell 56 (2021) 723–725.","ama":"Gärtner FR, Sixt MK. Engaging the front wheels to drive through fibrous terrain. <i>Developmental Cell</i>. 2021;56(6):723-725. doi:<a href=\"https://doi.org/10.1016/j.devcel.2021.03.002\">10.1016/j.devcel.2021.03.002</a>","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.” <i>Developmental Cell</i>, vol. 56, no. 6, Elsevier, 2021, pp. 723–25, doi:<a href=\"https://doi.org/10.1016/j.devcel.2021.03.002\">10.1016/j.devcel.2021.03.002</a>.","apa":"Gärtner, F. R., &#38; Sixt, M. K. (2021). Engaging the front wheels to drive through fibrous terrain. <i>Developmental Cell</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.devcel.2021.03.002\">https://doi.org/10.1016/j.devcel.2021.03.002</a>"},"issue":"6","fulldoi":"https://doi.org/10.1016/j.devcel.2021.03.002","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."}],"day":"22","quality_controlled":"1","_id":"9294","doi":"10.1016/j.devcel.2021.03.002","publisher":"Elsevier","department":[{"_id":"MiSi"}],"publication":"Developmental Cell","status":"public","page":"723-725","language":[{"iso":"eng"}],"author":[{"id":"397A88EE-F248-11E8-B48F-1D18A9856A87","full_name":"Gärtner, Florian R","orcid":"0000-0001-6120-3723","last_name":"Gärtner","first_name":"Florian R"},{"first_name":"Michael K","full_name":"Sixt, Michael K","orcid":"0000-0002-6620-9179","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","last_name":"Sixt"}],"publication_status":"published","title":"Engaging the front wheels to drive through fibrous terrain","intvolume":"        56","article_processing_charge":"No","pmid":1,"volume":56,"date_published":"2021-03-22T00:00:00Z"},{"year":"2021","project":[{"_id":"25FE9508-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","name":"Cellular Navigation Along Spatial Gradients","grant_number":"724373"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"eissn":["1944-8252"],"issn":["1944-8244"]},"type":"journal_article","corr_author":"1","tmp":{"image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)"},"scopus_import":"1","oa_version":"Published Version","external_id":{"isi":["000683741400026"],"pmid":["34283577"]},"month":"08","date_updated":"2025-07-10T12:02:02Z","isi":1,"article_type":"original","ddc":["620","570"],"file":[{"checksum":"b043a91d9f9200e467b970b692687ed3","creator":"asandaue","date_created":"2021-08-09T09:44:03Z","success":1,"content_type":"application/pdf","file_size":7123293,"access_level":"open_access","relation":"main_file","file_id":"9833","date_updated":"2021-08-09T09:44:03Z","file_name":"2021_ACSAppliedMaterialsAndInterfaces_Zisis.pdf"}],"date_created":"2021-08-08T22:01:28Z","oa":1,"citation":{"ieee":"T. Zisis <i>et al.</i>, “Sequential and switchable patterning for studying cellular processes under spatiotemporal control,” <i>ACS Applied Materials and Interfaces</i>, vol. 13, no. 30. American Chemical Society, pp. 35545–35560, 2021.","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.” <i>ACS Applied Materials and Interfaces</i>. American Chemical Society, 2021. <a href=\"https://doi.org/10.1021/acsami.1c09850\">https://doi.org/10.1021/acsami.1c09850</a>.","ama":"Zisis T, Schwarz J, Balles M, et al. Sequential and switchable patterning for studying cellular processes under spatiotemporal control. <i>ACS Applied Materials and Interfaces</i>. 2021;13(30):35545–35560. doi:<a href=\"https://doi.org/10.1021/acsami.1c09850\">10.1021/acsami.1c09850</a>","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.","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. <i>ACS Applied Materials and Interfaces</i>. American Chemical Society. <a href=\"https://doi.org/10.1021/acsami.1c09850\">https://doi.org/10.1021/acsami.1c09850</a>","mla":"Zisis, Themistoklis, et al. “Sequential and Switchable Patterning for Studying Cellular Processes under Spatiotemporal Control.” <i>ACS Applied Materials and Interfaces</i>, vol. 13, no. 30, American Chemical Society, 2021, pp. 35545–35560, doi:<a href=\"https://doi.org/10.1021/acsami.1c09850\">10.1021/acsami.1c09850</a>.","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."},"has_accepted_license":"1","fulldoi":"https://doi.org/10.1021/acsami.1c09850","issue":"30","quality_controlled":"1","abstract":[{"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.","lang":"eng"}],"day":"04","_id":"9822","file_date_updated":"2021-08-09T09:44:03Z","doi":"10.1021/acsami.1c09850","publisher":"American Chemical Society","publication":"ACS Applied Materials and Interfaces","page":"35545–35560","status":"public","ec_funded":1,"department":[{"_id":"MiSi"},{"_id":"GaTk"},{"_id":"Bio"},{"_id":"CaGu"}],"language":[{"iso":"eng"}],"intvolume":"        13","title":"Sequential and switchable patterning for studying cellular processes under spatiotemporal control","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)","author":[{"last_name":"Zisis","full_name":"Zisis, Themistoklis","first_name":"Themistoklis"},{"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"},{"id":"34E27F1C-F248-11E8-B48F-1D18A9856A87","last_name":"Nemethova","full_name":"Nemethova, Maria","first_name":"Maria"},{"first_name":"Remy P","last_name":"Chait","orcid":"0000-0003-0876-3187","id":"3464AE84-F248-11E8-B48F-1D18A9856A87","full_name":"Chait, Remy P"},{"first_name":"Robert","orcid":"0000-0001-9843-3522","last_name":"Hauschild","full_name":"Hauschild, Robert","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Janina","last_name":"Lange","full_name":"Lange, Janina"},{"full_name":"Guet, Calin C","id":"47F8433E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-6220-2052","last_name":"Guet","first_name":"Calin C"},{"last_name":"Sixt","orcid":"0000-0002-4561-241X","full_name":"Sixt, Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","first_name":"Michael K"},{"first_name":"Stefan","last_name":"Zahler","full_name":"Zahler, Stefan"}],"publication_status":"published","volume":13,"date_published":"2021-08-04T00:00:00Z","pmid":1},{"has_accepted_license":"1","fulldoi":"https://doi.org/10.1038/s41467-021-23123-x","issue":"1","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."}],"day":"24","quality_controlled":"1","_id":"9429","keyword":["General Biochemistry","Genetics and Molecular Biology"],"file_date_updated":"2021-05-28T12:39:43Z","doi":"10.1038/s41467-021-23123-x","publisher":"Springer Nature","ec_funded":1,"department":[{"_id":"GaNo"},{"_id":"JoDa"},{"_id":"FlSc"},{"_id":"MiSi"},{"_id":"LifeSc"},{"_id":"Bio"}],"publication":"Nature Communications","article_number":"3058","status":"public","related_material":{"link":[{"relation":"press_release","url":"https://ist.ac.at/en/news/defective-gene-slows-down-brain-cells/"}],"record":[{"id":"19557","relation":"dissertation_contains","status":"public"},{"id":"7800","relation":"earlier_version","status":"public"},{"id":"12401","relation":"dissertation_contains","status":"public"}]},"language":[{"iso":"eng"}],"author":[{"full_name":"Morandell, Jasmin","last_name":"Morandell","id":"4739D480-F248-11E8-B48F-1D18A9856A87","first_name":"Jasmin"},{"first_name":"Lena A","last_name":"Schwarz","id":"29A8453C-F248-11E8-B48F-1D18A9856A87","full_name":"Schwarz, Lena A"},{"first_name":"Bernadette","last_name":"Basilico","id":"36035796-5ACA-11E9-A75E-7AF2E5697425","full_name":"Basilico, Bernadette","orcid":"0000-0003-1843-3173"},{"first_name":"Saren","last_name":"Tasciyan","orcid":"0000-0003-1671-393X","full_name":"Tasciyan, Saren","id":"4323B49C-F248-11E8-B48F-1D18A9856A87"},{"id":"38C393BE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8370-6161","full_name":"Dimchev, Georgi A","last_name":"Dimchev","first_name":"Georgi A"},{"full_name":"Nicolas, Armel","last_name":"Nicolas","id":"2A103192-F248-11E8-B48F-1D18A9856A87","first_name":"Armel"},{"id":"4DF26D8C-F248-11E8-B48F-1D18A9856A87","full_name":"Sommer, Christoph M","last_name":"Sommer","orcid":"0000-0003-1216-9105","first_name":"Christoph M"},{"first_name":"Caroline","last_name":"Kreuzinger","full_name":"Kreuzinger, Caroline","id":"382077BA-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Dotter, Christoph","orcid":"0000-0002-9033-9096","id":"4C66542E-F248-11E8-B48F-1D18A9856A87","last_name":"Dotter","first_name":"Christoph"},{"first_name":"Lisa","full_name":"Knaus, Lisa","id":"3B2ABCF4-F248-11E8-B48F-1D18A9856A87","last_name":"Knaus"},{"first_name":"Zoe","full_name":"Dobler, Zoe","last_name":"Dobler","id":"D23090A2-9057-11EA-883A-A8396FC7A38F"},{"first_name":"Emanuele","last_name":"Cacci","full_name":"Cacci, Emanuele"},{"first_name":"Florian KM","id":"48AD8942-F248-11E8-B48F-1D18A9856A87","full_name":"Schur, Florian KM","last_name":"Schur","orcid":"0000-0003-4790-8078"},{"first_name":"Johann G","full_name":"Danzl, Johann G","last_name":"Danzl","orcid":"0000-0001-8559-3973","id":"42EFD3B6-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Gaia","orcid":"0000-0002-7673-7178","id":"3E57A680-F248-11E8-B48F-1D18A9856A87","full_name":"Novarino, Gaia","last_name":"Novarino"}],"publication_status":"published","intvolume":"        12","title":"Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development","article_processing_charge":"No","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).","volume":12,"date_published":"2021-05-24T00:00:00Z","acknowledged_ssus":[{"_id":"PreCl"}],"project":[{"call_identifier":"H2020","name":"ISTplus - Postdoctoral Fellowships","grant_number":"754411","_id":"260C2330-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":"25444568-B435-11E9-9278-68D0E5697425"},{"grant_number":"W1232","name":"Molecular Drug Targets","call_identifier":"FWF","_id":"2548AE96-B435-11E9-9278-68D0E5697425"},{"grant_number":"F7807","name":"Stem Cell Modulation in Neural Development and Regeneration/ P07-Neural stem cells in autism and epilepsy","_id":"05A0D778-7A3F-11EA-A408-12923DDC885E"},{"_id":"265CB4D0-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"I03600","name":"Optical control of synaptic function via adhesion molecules"}],"year":"2021","corr_author":"1","type":"journal_article","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","publication_identifier":{"eissn":["2041-1723"]},"tmp":{"image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)"},"scopus_import":"1","oa_version":"Published Version","month":"05","external_id":{"isi":["000658769900010"]},"article_type":"original","isi":1,"date_updated":"2026-09-28T22:30:13Z","ddc":["572"],"file":[{"file_id":"9430","date_updated":"2021-05-28T12:39:43Z","file_name":"2021_NatureCommunications_Morandell.pdf","relation":"main_file","date_created":"2021-05-28T12:39:43Z","success":1,"content_type":"application/pdf","file_size":9358599,"access_level":"open_access","checksum":"337e0f7959c35ec959984cacdcb472ba","creator":"kschuh"}],"date_created":"2021-05-28T11:49:46Z","oa":1,"citation":{"ieee":"J. Morandell <i>et al.</i>, “Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development,” <i>Nature Communications</i>, vol. 12, no. 1. Springer Nature, 2021.","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.” <i>Nature Communications</i>. Springer Nature, 2021. <a href=\"https://doi.org/10.1038/s41467-021-23123-x\">https://doi.org/10.1038/s41467-021-23123-x</a>.","ama":"Morandell J, Schwarz LA, Basilico B, et al. Cul3 regulates cytoskeleton protein homeostasis and cell migration during a critical window of brain development. <i>Nature Communications</i>. 2021;12(1). doi:<a href=\"https://doi.org/10.1038/s41467-021-23123-x\">10.1038/s41467-021-23123-x</a>","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).","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.","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. <i>Nature Communications</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41467-021-23123-x\">https://doi.org/10.1038/s41467-021-23123-x</a>","mla":"Morandell, Jasmin, et al. “Cul3 Regulates Cytoskeleton Protein Homeostasis and Cell Migration during a Critical Window of Brain Development.” <i>Nature Communications</i>, vol. 12, no. 1, 3058, Springer Nature, 2021, doi:<a href=\"https://doi.org/10.1038/s41467-021-23123-x\">10.1038/s41467-021-23123-x</a>."}},{"year":"2021","publication_identifier":{"issn":["2663-337X"]},"user_id":"ba8df636-2132-11f1-aed0-ed93e2281fdd","corr_author":"1","type":"dissertation","alternative_title":["ISTA Thesis"],"oa_version":"Published Version","month":"11","supervisor":[{"first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-4561-241X","full_name":"Sixt, Michael K","last_name":"Sixt"},{"first_name":"Calin C","id":"47F8433E-F248-11E8-B48F-1D18A9856A87","last_name":"Guet","full_name":"Guet, Calin C","orcid":"0000-0001-6220-2052"}],"date_updated":"2026-07-06T12:48:19Z","ddc":["570"],"file":[{"checksum":"b39c9e0ef18d0484d537a67551effd02","creator":"ktomasek","date_created":"2021-11-18T15:07:31Z","access_level":"open_access","content_type":"application/pdf","file_size":13266088,"embargo":"2022-11-18","relation":"main_file","file_id":"10308","date_updated":"2022-12-20T23:30:05Z","file_name":"ThesisTomasekKathrin.pdf"},{"date_created":"2021-11-18T15:07:46Z","access_level":"closed","file_size":7539509,"content_type":"application/vnd.openxmlformats-officedocument.wordprocessingml.document","checksum":"c0c440ee9e5ef1102a518a4f9f023e7c","embargo_to":"open_access","creator":"ktomasek","file_id":"10309","date_updated":"2022-12-20T23:30:05Z","file_name":"ThesisTomasekKathrin.docx","relation":"source_file"}],"date_created":"2021-11-18T15:05:06Z","oa":1,"citation":{"short":"K. Tomasek, Pathogenic Escherichia Coli Hijack the Host Immune Response, Institute of Science and Technology Austria, 2021.","ama":"Tomasek K. Pathogenic Escherichia coli hijack the host immune response. 2021. doi:<a href=\"https://doi.org/10.15479/at:ista:10307\">10.15479/at:ista:10307</a>","ista":"Tomasek K. 2021. Pathogenic Escherichia coli hijack the host immune response. Institute of Science and Technology Austria.","mla":"Tomasek, Kathrin. <i>Pathogenic Escherichia Coli Hijack the Host Immune Response</i>. Institute of Science and Technology Austria, 2021, doi:<a href=\"https://doi.org/10.15479/at:ista:10307\">10.15479/at:ista:10307</a>.","apa":"Tomasek, K. (2021). <i>Pathogenic Escherichia coli hijack the host immune response</i>. Institute of Science and Technology Austria. <a href=\"https://doi.org/10.15479/at:ista:10307\">https://doi.org/10.15479/at:ista:10307</a>","ieee":"K. Tomasek, “Pathogenic Escherichia coli hijack the host immune response,” Institute of Science and Technology Austria, 2021.","chicago":"Tomasek, Kathrin. “Pathogenic Escherichia Coli Hijack the Host Immune Response.” Institute of Science and Technology Austria, 2021. <a href=\"https://doi.org/10.15479/at:ista:10307\">https://doi.org/10.15479/at:ista:10307</a>."},"fulldoi":"https://doi.org/10.15479/at:ista:10307","has_accepted_license":"1","abstract":[{"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.","lang":"eng"}],"day":"18","_id":"10307","file_date_updated":"2022-12-20T23:30:05Z","doi":"10.15479/at:ista:10307","degree_awarded":"PhD","publisher":"Institute of Science and Technology Austria","OA_place":"publisher","status":"public","page":"73","department":[{"_id":"MiSi"},{"_id":"CaGu"},{"_id":"GradSch"}],"related_material":{"record":[{"id":"10316","relation":"part_of_dissertation","status":"public"}]},"language":[{"iso":"eng"}],"title":"Pathogenic Escherichia coli hijack the host immune response","article_processing_charge":"No","publication_status":"published","author":[{"id":"3AEC8556-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-3768-877X","last_name":"Tomasek","full_name":"Tomasek, Kathrin","first_name":"Kathrin"}],"acknowledged_ssus":[{"_id":"LifeSc"},{"_id":"Bio"},{"_id":"PreCl"},{"_id":"EM-Fac"}],"date_published":"2021-11-18T00:00:00Z"}]