--- OA_place: publisher OA_type: gold _id: '14647' abstract: - lang: eng text: "In the developing vertebrate central nervous system, neurons and glia typically arise\r\nsequentially from common progenitors. Here, we report that the transcription factor Forkhead\r\nBox G1 (Foxg1) regulates gliogenesis in the mouse neocortex via distinct cell-autonomous roles in progenitors and postmitotic neurons that regulate different aspects of the gliogenic FGF signalling pathway. We demonstrate that loss of Foxg1 in cortical progenitors at neurogenic stages causes premature astrogliogenesis. We identify a novel FOXG1 target, the pro-gliogenic FGF pathway component Fgfr3, which is suppressed by FOXG1 cell-autonomously to maintain neurogenesis. Furthermore, FOXG1 can also suppress premature astrogliogenesis triggered by the augmentation of FGF signalling. We identify a second novel function of FOXG1 in regulating the expression of gliogenic cues in newborn neocortical upper-layer neurons. Loss of FOXG1 in postmitotic neurons non-autonomously enhances gliogenesis in the progenitors via FGF signalling. These results fit well with the model that newborn neurons secrete cues that trigger progenitors to produce the next wave of cell types, astrocytes. If FGF signalling is attenuated in Foxg1 null progenitors, they progress to oligodendrocyte production. Therefore, loss of FOXG1 transitions the progenitor to a gliogenic state, producing either astrocytes or oligodendrocytes depending on FGF signalling levels. Our results uncover how FOXG1 integrates extrinsic signalling via the FGF pathway to regulate the sequential generation of neurons, astrocytes, and oligodendrocytes in the cerebral cortex. " acknowledgement: "We thank the animal house staff of the Tata Institute of Fundamental Research, Mumbai (TIFR), for their excellent support; Gordon Fishell (Harvard Medical School, USA), and Goichi Miyoshi (Gunma University, Japan) for the Foxg1 floxed mouse line; Hiroshi Kawasaki (Kanazawa University, Japan) for the plasmids pCAG-FGF8 and pCAG-sFgfr3c; Soo Kyung Lee (University at Buffalo, The State University of New York, USA) for the Foxg1lox/lox genotyping primers and protocol. We thank Deepak Modi and Vainav Patel (National Institute for Research in Reproductive and Child Health, NIRRCH, Mumbai, India) for the use of the NIRRCH FACS Facility, and the staff of the NIRRCH and TIFR FACS facilities for their assistance. We thank Denis Jabaudon (University of Geneva, Switzerland) for his critical comments on the manuscript and members of the Jabaudon lab for helpful discussions. This work was funded by the Department of Atomic Energy (DAE), Govt. of India (Project Identification no. RTI4003,\r\nDAE OM no. 1303/2/2019/R&D-II/DAE/2079). " article_number: '101851' article_processing_charge: Yes article_type: original author: - first_name: Mahima full_name: Bose, Mahima last_name: Bose - first_name: Varun full_name: Suresh, Varun last_name: Suresh - first_name: Urvi full_name: Mishra, Urvi last_name: Mishra - first_name: Ishita full_name: Talwar, Ishita last_name: Talwar - first_name: Anuradha full_name: Yadav, Anuradha last_name: Yadav - first_name: Shiona full_name: Biswas, Shiona last_name: Biswas - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Shubha full_name: Tole, Shubha last_name: Tole citation: ama: Bose M, Suresh V, Mishra U, et al. Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway. eLife. 2025;13. doi:10.7554/elife.101851.3 apa: Bose, M., Suresh, V., Mishra, U., Talwar, I., Yadav, A., Biswas, S., … Tole, S. (2025). Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.101851.3 chicago: Bose, Mahima, Varun Suresh, Urvi Mishra, Ishita Talwar, Anuradha Yadav, Shiona Biswas, Simon Hippenmeyer, and Shubha Tole. “Dual Role of FOXG1 in Regulating Gliogenesis in the Developing Neocortex via the FGF Signalling Pathway.” ELife. eLife Sciences Publications, 2025. https://doi.org/10.7554/elife.101851.3. ieee: M. Bose et al., “Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway,” eLife, vol. 13. eLife Sciences Publications, 2025. ista: Bose M, Suresh V, Mishra U, Talwar I, Yadav A, Biswas S, Hippenmeyer S, Tole S. 2025. Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway. eLife. 13, 101851. mla: Bose, Mahima, et al. “Dual Role of FOXG1 in Regulating Gliogenesis in the Developing Neocortex via the FGF Signalling Pathway.” ELife, vol. 13, 101851, eLife Sciences Publications, 2025, doi:10.7554/elife.101851.3. short: M. Bose, V. Suresh, U. Mishra, I. Talwar, A. Yadav, S. Biswas, S. Hippenmeyer, S. Tole, ELife 13 (2025). date_created: 2023-12-06T13:07:01Z date_published: 2025-03-14T00:00:00Z date_updated: 2025-05-14T11:41:52Z day: '14' ddc: - '570' department: - _id: SiHi doi: 10.7554/elife.101851.3 external_id: pmid: - '40085500' file: - access_level: open_access checksum: 64a6a6f86e24b21fe72c7a7fd6056fed content_type: application/pdf creator: dernst date_created: 2025-04-03T11:19:26Z date_updated: 2025-04-03T11:19:26Z file_id: '19467' file_name: 2025_eLife_Bose.pdf file_size: 17462771 relation: main_file success: 1 file_date_updated: 2025-04-03T11:19:26Z has_accepted_license: '1' intvolume: ' 13' language: - iso: eng license: https://creativecommons.org/licenses/by/4.0/ month: '03' oa: 1 oa_version: Published Version pmid: 1 publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via the FGF signalling pathway tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 13 year: '2025' ... --- DOAJ_listed: '1' OA_place: publisher OA_type: gold PlanS_conform: '1' _id: '21251' abstract: - lang: eng text: Cellular membranes differ across the tree of life. In most bacteria and eukaryotes, single-headed lipids self-assemble into flexible bilayer membranes. By contrast, thermophilic archaea tend to possess bilayer lipids together with double-headed, monolayer spanning bolalipids, which are thought to enable cells to survive in harsh environments. Here, using a minimal computational model for bolalipid membranes, we explore the trade-offs at play when forming membranes. We find that flexible bolalipids form membranes that resemble bilayer membranes because they are able to assume a U-shaped conformation. Conversely, rigid bolalipids, which resemble the bolalipids with cyclic groups found in thermophilic archaea, take on a straight conformation and form membranes that are stiff and prone to pore formation when they undergo changes in shape. Strikingly, however, the inclusion of small amounts of bilayer lipids in a bolalipid membrane is enough to achieve fluid bolalipid membranes that are both stable and flexible, resolving this trade-off. Our study suggests a mechanism by which archaea can tune the material properties of their membranes as and when required to enable them to survive in harsh environments and to undergo essential membrane remodelling events like cell division. acknowledgement: MA, BB, and AŠ acknowledge funding by the Volkswagen Foundation Grant Az 96727. FF acknowledges financial support by the NOMIS foundation. AŠ acknowledges funding by ERC Starting Grant 'NEPA' 802960. We thank Claudia Flandoli for her help with illustrations. article_number: '105432' article_processing_charge: Yes article_type: original author: - first_name: Miguel full_name: Santana de Freitas Amaral, Miguel id: 4f2d02dd-47a9-11ec-ad10-82820ed3f501 last_name: Santana de Freitas Amaral - first_name: Felix F full_name: Frey, Felix F id: a0270b37-8f1a-11ec-95c7-8e710c59a4f3 last_name: Frey orcid: 0000-0001-8501-6017 - first_name: Xiuyun full_name: Jiang, Xiuyun last_name: Jiang - first_name: Buzz full_name: Baum, Buzz last_name: Baum - first_name: Anđela full_name: Šarić, Anđela id: bf63d406-f056-11eb-b41d-f263a6566d8b last_name: Šarić orcid: 0000-0002-7854-2139 citation: ama: Santana de Freitas Amaral M, Frey FF, Jiang X, Baum B, Šarić A. Balancing stability and flexibility when reshaping archaeal membranes. eLife. 2025;14. doi:10.7554/elife.105432 apa: Santana de Freitas Amaral, M., Frey, F. F., Jiang, X., Baum, B., & Šarić, A. (2025). Balancing stability and flexibility when reshaping archaeal membranes. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.105432 chicago: Santana de Freitas Amaral, Miguel, Felix F Frey, Xiuyun Jiang, Buzz Baum, and Anđela Šarić. “Balancing Stability and Flexibility When Reshaping Archaeal Membranes.” ELife. eLife Sciences Publications, 2025. https://doi.org/10.7554/elife.105432. ieee: M. Santana de Freitas Amaral, F. F. Frey, X. Jiang, B. Baum, and A. Šarić, “Balancing stability and flexibility when reshaping archaeal membranes,” eLife, vol. 14. eLife Sciences Publications, 2025. ista: Santana de Freitas Amaral M, Frey FF, Jiang X, Baum B, Šarić A. 2025. Balancing stability and flexibility when reshaping archaeal membranes. eLife. 14, 105432. mla: Santana de Freitas Amaral, Miguel, et al. “Balancing Stability and Flexibility When Reshaping Archaeal Membranes.” ELife, vol. 14, 105432, eLife Sciences Publications, 2025, doi:10.7554/elife.105432. short: M. Santana de Freitas Amaral, F.F. Frey, X. Jiang, B. Baum, A. Šarić, ELife 14 (2025). corr_author: '1' date_created: 2026-02-16T15:43:57Z date_published: 2025-10-07T00:00:00Z date_updated: 2026-02-23T11:49:05Z day: '07' ddc: - '570' department: - _id: AnSa doi: 10.7554/elife.105432 ec_funded: 1 external_id: pmid: - '41056191 ' file: - access_level: open_access checksum: 4116cd5143558ded995fb9ff5fcbc7e0 content_type: application/pdf creator: dernst date_created: 2026-02-17T13:02:02Z date_updated: 2026-02-17T13:02:02Z file_id: '21305' file_name: 2025_elife_Amaral.pdf file_size: 10668225 relation: main_file success: 1 file_date_updated: 2026-02-17T13:02:02Z has_accepted_license: '1' intvolume: ' 14' language: - iso: eng month: '10' oa: 1 oa_version: Published Version pmid: 1 project: - _id: eba2549b-77a9-11ec-83b8-a81e493eae4e call_identifier: H2020 grant_number: '802960' name: 'Non-Equilibrium Protein Assembly: from Building Blocks to Biological Machines' publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' related_material: record: - id: '21304' relation: software status: public status: public title: Balancing stability and flexibility when reshaping archaeal membranes tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 14 year: '2025' ... --- DOAJ_listed: '1' OA_place: publisher OA_type: gold _id: '20808' abstract: - lang: eng text: During Caenorhabditis elegans development, multiple cells migrate long distances or extend processes to reach their final position and/or attain proper shape. The Wnt signalling pathway stands out as one of the major coordinators of cell migration or cell outgrowth along the anterior-posterior body axis. The outcome of Wnt signalling is fine-tuned by various mechanisms including endocytosis. In this study, we show that SEL-5, the C. elegans orthologue of mammalian AP2-associated kinase AAK1, acts together with the retromer complex as a positive regulator of EGL-20/Wnt signalling during the migration of QL neuroblast daughter cells. At the same time, SEL-5 in cooperation with the retromer complex is also required during excretory canal cell outgrowth. Importantly, SEL-5 kinase activity is not required for its role in neuronal migration or excretory cell outgrowth, and neither of these processes is dependent on DPY-23/AP2M1 phosphorylation. We further establish that the Wnt proteins CWN-1 and CWN-2, together with the Frizzled receptor CFZ-2, positively regulate excretory cell outgrowth, while LIN-44/Wnt and LIN-17/Frizzled together generate a stop signal inhibiting its extension. article_number: e91054 article_processing_charge: Yes article_type: original author: - first_name: Filip full_name: Knop, Filip id: 25f3131f-6e7c-11ef-8296-b64ccd4a1b69 last_name: Knop orcid: 0000-0002-3845-3465 - first_name: Apolena full_name: Zounarová, Apolena last_name: Zounarová - first_name: Vojtěch full_name: Šabata, Vojtěch last_name: Šabata - first_name: Teije Corneel full_name: Middelkoop, Teije Corneel last_name: Middelkoop - first_name: Marie full_name: Macůrková, Marie last_name: Macůrková citation: ama: Knop F, Zounarová A, Šabata V, Middelkoop TC, Macůrková M. Caenorhabditis elegans SEL-5/AAK1 regulates cell migration and cell outgrowth independently of its kinase activity. eLife. 2024;13. doi:10.7554/elife.91054 apa: Knop, F., Zounarová, A., Šabata, V., Middelkoop, T. C., & Macůrková, M. (2024). Caenorhabditis elegans SEL-5/AAK1 regulates cell migration and cell outgrowth independently of its kinase activity. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.91054 chicago: Knop, Filip, Apolena Zounarová, Vojtěch Šabata, Teije Corneel Middelkoop, and Marie Macůrková. “Caenorhabditis Elegans SEL-5/AAK1 Regulates Cell Migration and Cell Outgrowth Independently of Its Kinase Activity.” ELife. eLife Sciences Publications, 2024. https://doi.org/10.7554/elife.91054. ieee: F. Knop, A. Zounarová, V. Šabata, T. C. Middelkoop, and M. Macůrková, “Caenorhabditis elegans SEL-5/AAK1 regulates cell migration and cell outgrowth independently of its kinase activity,” eLife, vol. 13. eLife Sciences Publications, 2024. ista: Knop F, Zounarová A, Šabata V, Middelkoop TC, Macůrková M. 2024. Caenorhabditis elegans SEL-5/AAK1 regulates cell migration and cell outgrowth independently of its kinase activity. eLife. 13, e91054. mla: Knop, Filip, et al. “Caenorhabditis Elegans SEL-5/AAK1 Regulates Cell Migration and Cell Outgrowth Independently of Its Kinase Activity.” ELife, vol. 13, e91054, eLife Sciences Publications, 2024, doi:10.7554/elife.91054. short: F. Knop, A. Zounarová, V. Šabata, T.C. Middelkoop, M. Macůrková, ELife 13 (2024). date_created: 2025-12-12T09:06:31Z date_published: 2024-07-19T00:00:00Z date_updated: 2025-12-15T10:26:56Z day: '19' doi: 10.7554/elife.91054 extern: '1' external_id: pmid: - '39028260' intvolume: ' 13' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.7554/elife.91054 month: '07' oa: 1 oa_version: Published Version pmid: 1 publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Caenorhabditis elegans SEL-5/AAK1 regulates cell migration and cell outgrowth independently of its kinase activity type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 13 year: '2024' ... --- DOAJ_listed: '1' OA_place: publisher OA_type: gold _id: '18757' abstract: - lang: eng text: 'Segmentation is a critical data processing step in many applications of cryo-electron tomography. Downstream analyses, such as subtomogram averaging, are often based on segmentation results, and are thus critically dependent on the availability of open-source software for accurate as well as high-throughput tomogram segmentation. There is a need for more user-friendly, flexible, and comprehensive segmentation software that offers an insightful overview of all steps involved in preparing automated segmentations. Here, we present Ais: a dedicated tomogram segmentation package that is geared towards both high performance and accessibility, available on GitHub. In this report, we demonstrate two common processing steps that can be greatly accelerated with Ais: particle picking for subtomogram averaging, and generating many-feature segmentations of cellular architecture based on in situ tomography data. Featuring comprehensive annotation, segmentation, and rendering functionality, as well as an open repository for trained models at aiscryoet.org, we hope that Ais will help accelerate research and dissemination of data involving cryoET.' acknowledgement: 'We thank A Koster and M Barcena for helpful discussions and kindly sharing the coronaviral replication organelle datasets. We are also grateful to van den Hoek et al., 2022 and Wu et al., 2023, for uploading the data that we used for Figure 5 onto EMPIAR and EMDB, as well as to the authors of various other datasets uploaded to these databases that are not discussed in this manuscript but that were useful for testing the software. We also thank the reviewers, whose comments were very helpful in improving the manuscript and the software. Finally, we are grateful the early Ais users who provided us with feedback on the software and reported issues. This research was supported by the following grants to THS: European Research Council H202 Grant 759517; European Union’s Horizon Europe Program IMAGINE grant 101094250, and the Netherlands Organization for Scientific Research Grant VI.Vidi.193.014.' article_number: '98552' article_processing_charge: Yes article_type: original author: - first_name: Mart G.F. full_name: Last, Mart G.F. last_name: Last - first_name: Leoni full_name: Abendstein, Leoni id: 14f1f051-cd9d-11ef-9c94-8b942a882560 last_name: Abendstein orcid: 0000-0001-7634-5353 - first_name: Lenard M. full_name: Voortman, Lenard M. last_name: Voortman - first_name: Thomas H. full_name: Sharp, Thomas H. last_name: Sharp citation: ama: Last MGF, Abendstein L, Voortman LM, Sharp TH. Streamlining segmentation of cryo-electron tomography datasets with Ais. eLife. 2024;13. doi:10.7554/eLife.98552 apa: Last, M. G. F., Abendstein, L., Voortman, L. M., & Sharp, T. H. (2024). Streamlining segmentation of cryo-electron tomography datasets with Ais. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.98552 chicago: Last, Mart G.F., Leoni Abendstein, Lenard M. Voortman, and Thomas H. Sharp. “Streamlining Segmentation of Cryo-Electron Tomography Datasets with Ais.” ELife. eLife Sciences Publications, 2024. https://doi.org/10.7554/eLife.98552. ieee: M. G. F. Last, L. Abendstein, L. M. Voortman, and T. H. Sharp, “Streamlining segmentation of cryo-electron tomography datasets with Ais,” eLife, vol. 13. eLife Sciences Publications, 2024. ista: Last MGF, Abendstein L, Voortman LM, Sharp TH. 2024. Streamlining segmentation of cryo-electron tomography datasets with Ais. eLife. 13, 98552. mla: Last, Mart G. F., et al. “Streamlining Segmentation of Cryo-Electron Tomography Datasets with Ais.” ELife, vol. 13, 98552, eLife Sciences Publications, 2024, doi:10.7554/eLife.98552. short: M.G.F. Last, L. Abendstein, L.M. Voortman, T.H. Sharp, ELife 13 (2024). date_created: 2025-01-05T23:01:57Z date_published: 2024-12-20T00:00:00Z date_updated: 2025-01-08T08:52:51Z day: '20' ddc: - '570' department: - _id: FlPr doi: 10.7554/eLife.98552 external_id: pmid: - '39704648' file: - access_level: open_access checksum: a4f0f906e4d5c1078208b317e78699d1 content_type: application/pdf creator: dernst date_created: 2025-01-08T08:51:45Z date_updated: 2025-01-08T08:51:45Z file_id: '18774' file_name: 2024_eLife_Last.pdf file_size: 7445664 relation: main_file success: 1 file_date_updated: 2025-01-08T08:51:45Z has_accepted_license: '1' intvolume: ' 13' language: - iso: eng month: '12' oa: 1 oa_version: Published Version pmid: 1 publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Streamlining segmentation of cryo-electron tomography datasets with Ais tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 13 year: '2024' ... --- _id: '14315' abstract: - lang: eng text: During apoptosis, caspases degrade 8 out of ~30 nucleoporins to irreversibly demolish the nuclear pore complex. However, for poorly understood reasons, caspases are also activated during cell differentiation. Here, we show that sublethal activation of caspases during myogenesis results in the transient proteolysis of four peripheral Nups and one transmembrane Nup. ‘Trimmed’ NPCs become nuclear export-defective, and we identified in an unbiased manner several classes of cytoplasmic, plasma membrane, and mitochondrial proteins that rapidly accumulate in the nucleus. NPC trimming by non-apoptotic caspases was also observed in neurogenesis and endoplasmic reticulum stress. Our results suggest that caspases can reversibly modulate nuclear transport activity, which allows them to function as agents of cell differentiation and adaptation at sublethal levels. acknowledgement: 'We thank the members of the Hetzer laboratory, Tony Hunter (Salk), Lorenzo Puri (Sanford Burnham Prebys), and Jongmin Kim (Massachusetts General Hospital) for the critical reading of the manuscript; Kenneth Diffenderfer and Aimee Pankonin (Stem Cell Core at the Salk Institute) for help with neurogenesis; Carol Marchetto and Fred Gage (Salk) for providing H9 embryonic stem cells; Lorenzo Puri, Alexandra Sacco, and Luca Caputo (Sanford Burnham Prebys) for helpful discussions and sharing mouse primary myoblasts. This work was supported by a Glenn Foundation for Medical Research Postdoctoral Fellowship in Aging Research (UHC), the NOMIS foundation (MWH), and the National Institutes of Health (R01 NS096786 to MWH and K01 AR080828 to UHC). This work was also supported by the Mass Spectrometry Core of the Salk Institute with funding from NIH-NCI CCSG: P30 014195 and the Helmsley Center for Genomic Medicine. We thank Jolene Diedrich and Antonio Pinto for technical support.' article_number: RP89066 article_processing_charge: Yes article_type: original author: - first_name: Ukrae H. full_name: Cho, Ukrae H. last_name: Cho - first_name: Martin W full_name: Hetzer, Martin W id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed last_name: Hetzer orcid: 0000-0002-2111-992X citation: ama: Cho UH, Hetzer M. Caspase-mediated nuclear pore complex trimming in cell differentiation and endoplasmic reticulum stress. eLife. 2023;12. doi:10.7554/eLife.89066 apa: Cho, U. H., & Hetzer, M. (2023). Caspase-mediated nuclear pore complex trimming in cell differentiation and endoplasmic reticulum stress. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.89066 chicago: Cho, Ukrae H., and Martin Hetzer. “Caspase-Mediated Nuclear Pore Complex Trimming in Cell Differentiation and Endoplasmic Reticulum Stress.” ELife. eLife Sciences Publications, 2023. https://doi.org/10.7554/eLife.89066. ieee: U. H. Cho and M. Hetzer, “Caspase-mediated nuclear pore complex trimming in cell differentiation and endoplasmic reticulum stress,” eLife, vol. 12. eLife Sciences Publications, 2023. ista: Cho UH, Hetzer M. 2023. Caspase-mediated nuclear pore complex trimming in cell differentiation and endoplasmic reticulum stress. eLife. 12, RP89066. mla: Cho, Ukrae H., and Martin Hetzer. “Caspase-Mediated Nuclear Pore Complex Trimming in Cell Differentiation and Endoplasmic Reticulum Stress.” ELife, vol. 12, RP89066, eLife Sciences Publications, 2023, doi:10.7554/eLife.89066. short: U.H. Cho, M. Hetzer, ELife 12 (2023). corr_author: '1' date_created: 2023-09-10T22:01:11Z date_published: 2023-09-04T00:00:00Z date_updated: 2024-10-09T21:06:57Z day: '04' ddc: - '570' department: - _id: MaHe doi: 10.7554/eLife.89066 external_id: pmid: - '37665327' file: - access_level: open_access checksum: db24bf3d595507387b48d3799c33e289 content_type: application/pdf creator: dernst date_created: 2023-09-15T06:59:10Z date_updated: 2023-09-15T06:59:10Z file_id: '14336' file_name: 2023_eLife_Cho.pdf file_size: 3703097 relation: main_file success: 1 file_date_updated: 2023-09-15T06:59:10Z has_accepted_license: '1' intvolume: ' 12' language: - iso: eng month: '09' oa: 1 oa_version: Published Version pmid: 1 publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Caspase-mediated nuclear pore complex trimming in cell differentiation and endoplasmic reticulum stress tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 12 year: '2023' ... --- _id: '13316' abstract: - lang: eng text: Although budding yeast has been extensively used as a model organism for studying organelle functions and intracellular vesicle trafficking, whether it possesses an independent endocytic early/sorting compartment that sorts endocytic cargos to the endo-lysosomal pathway or the recycling pathway has long been unclear. The structure and properties of the endocytic early/sorting compartment differ significantly between organisms; in plant cells, the trans-Golgi network (TGN) serves this role, whereas in mammalian cells a separate intracellular structure performs this function. The yeast syntaxin homolog Tlg2p, widely localizing to the TGN and endosomal compartments, is presumed to act as a Q-SNARE for endocytic vesicles, but which compartment is the direct target for endocytic vesicles remained unanswered. Here we demonstrate by high-speed and high-resolution 4D imaging of fluorescently labeled endocytic cargos that the Tlg2p-residing compartment within the TGN functions as the early/sorting compartment. After arriving here, endocytic cargos are recycled to the plasma membrane or transported to the yeast Rab5-residing endosomal compartment through the pathway requiring the clathrin adaptors GGAs. Interestingly, Gga2p predominantly localizes at the Tlg2p-residing compartment, and the deletion of GGAs has little effect on another TGN region where Sec7p is present but suppresses dynamics of the Tlg2-residing early/sorting compartment, indicating that the Tlg2p- and Sec7p-residing regions are discrete entities in the mutant. Thus, the Tlg2p-residing region seems to serve as an early/sorting compartment and function independently of the Sec7p-residing region within the TGN. acknowledgement: 'This work was supported by JSPS KAKENHI grant #18K062291, and the Takeda Science Foundation to JYT., as well as JSPS KAKENHI grant #19K065710, the Takeda Science Foundation, and Life Science Foundation of Japan to JT.' article_number: e84850 article_processing_charge: Yes article_type: original author: - first_name: Junko Y. full_name: Toshima, Junko Y. last_name: Toshima - first_name: Ayana full_name: Tsukahara, Ayana last_name: Tsukahara - first_name: Makoto full_name: Nagano, Makoto last_name: Nagano - first_name: Takuro full_name: Tojima, Takuro last_name: Tojima - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 - first_name: Akihiko full_name: Nakano, Akihiko last_name: Nakano - first_name: Jiro full_name: Toshima, Jiro last_name: Toshima citation: ama: Toshima JY, Tsukahara A, Nagano M, et al. The yeast endocytic early/sorting compartment exists as an independent sub-compartment within the trans-Golgi network. eLife. 2023;12. doi:10.7554/eLife.84850 apa: Toshima, J. Y., Tsukahara, A., Nagano, M., Tojima, T., Siekhaus, D. E., Nakano, A., & Toshima, J. (2023). The yeast endocytic early/sorting compartment exists as an independent sub-compartment within the trans-Golgi network. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.84850 chicago: Toshima, Junko Y., Ayana Tsukahara, Makoto Nagano, Takuro Tojima, Daria E Siekhaus, Akihiko Nakano, and Jiro Toshima. “The Yeast Endocytic Early/Sorting Compartment Exists as an Independent Sub-Compartment within the Trans-Golgi Network.” ELife. eLife Sciences Publications, 2023. https://doi.org/10.7554/eLife.84850. ieee: J. Y. Toshima et al., “The yeast endocytic early/sorting compartment exists as an independent sub-compartment within the trans-Golgi network,” eLife, vol. 12. eLife Sciences Publications, 2023. ista: Toshima JY, Tsukahara A, Nagano M, Tojima T, Siekhaus DE, Nakano A, Toshima J. 2023. The yeast endocytic early/sorting compartment exists as an independent sub-compartment within the trans-Golgi network. eLife. 12, e84850. mla: Toshima, Junko Y., et al. “The Yeast Endocytic Early/Sorting Compartment Exists as an Independent Sub-Compartment within the Trans-Golgi Network.” ELife, vol. 12, e84850, eLife Sciences Publications, 2023, doi:10.7554/eLife.84850. short: J.Y. Toshima, A. Tsukahara, M. Nagano, T. Tojima, D.E. Siekhaus, A. Nakano, J. Toshima, ELife 12 (2023). date_created: 2023-07-30T22:01:02Z date_published: 2023-07-21T00:00:00Z date_updated: 2023-12-13T11:37:36Z day: '21' ddc: - '570' department: - _id: DaSi doi: 10.7554/eLife.84850 external_id: isi: - '001035372800001' pmid: - '37477116' file: - access_level: open_access checksum: 2af111a00cf5e3a956f7f0fd13199b15 content_type: application/pdf creator: dernst date_created: 2023-07-31T07:43:00Z date_updated: 2023-07-31T07:43:00Z file_id: '13324' file_name: 2023_eLife_Toshima.pdf file_size: 11980913 relation: main_file success: 1 file_date_updated: 2023-07-31T07:43:00Z has_accepted_license: '1' intvolume: ' 12' isi: 1 language: - iso: eng month: '07' oa: 1 oa_version: Published Version pmid: 1 publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: The yeast endocytic early/sorting compartment exists as an independent sub-compartment within the trans-Golgi network tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 12 year: '2023' ... --- _id: '11843' abstract: - lang: eng text: A key attribute of persistent or recurring bacterial infections is the ability of the pathogen to evade the host’s immune response. Many Enterobacteriaceae express type 1 pili, a pre-adapted virulence trait, to invade host epithelial cells and establish persistent infections. However, the molecular mechanisms and strategies by which bacteria actively circumvent the immune response of the host remain poorly understood. Here, we identified CD14, the major co-receptor for lipopolysaccharide detection, on mouse dendritic cells (DCs) as a binding partner of FimH, the protein located at the tip of the type 1 pilus of Escherichia coli. The FimH amino acids involved in CD14 binding are highly conserved across pathogenic and non-pathogenic strains. Binding of the pathogenic strain CFT073 to CD14 reduced DC migration by overactivation of integrins and blunted expression of co-stimulatory molecules by overactivating the NFAT (nuclear factor of activated T-cells) pathway, both rate-limiting factors of T cell activation. This response was binary at the single-cell level, but averaged in larger populations exposed to both piliated and non-piliated pathogens, presumably via the exchange of immunomodulatory cytokines. While defining an active molecular mechanism of immune evasion by pathogens, the interaction between FimH and CD14 represents a potential target to interfere with persistent and recurrent infections, such as urinary tract infections or Crohn’s disease. acknowledged_ssus: - _id: Bio - _id: PreCl - _id: EM-Fac acknowledgement: We thank Ulrich Dobrindt for providing UPEC strains CFT073, UTI89, and 536, Frank Assen, Vlad Gavra, Maximilian Götz, Bor Kavčič, Jonna Alanko, and Eva Kiermaier for help with experiments and Robert Hauschild, Julian Stopp, and Saren Tasciyan for help with data analysis. We thank the IST Austria Scientific Service Units, especially the Bioimaging facility, the Preclinical facility and the Electron microscopy facility for technical support, Jakob Wallner and all members of the Guet and Sixt lab for fruitful discussions and Daria Siekhaus for critically reading the manuscript. This work was supported by grants from the Austrian Research Promotion Agency (FEMtech 868984) to IG, the European Research Council (CoG 724373), and the Austrian Science Fund (FWF P29911) to MS. article_number: e78995 article_processing_charge: Yes article_type: original author: - first_name: Kathrin full_name: Tomasek, Kathrin id: 3AEC8556-F248-11E8-B48F-1D18A9856A87 last_name: Tomasek orcid: 0000-0003-3768-877X - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Ivana full_name: Glatzová, Ivana id: 727b3c7d-4939-11ec-89b3-b9b0750ab74d last_name: Glatzová - first_name: Michael S. full_name: Lukesch, Michael S. last_name: Lukesch - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. eLife. 2022;11. doi:10.7554/eLife.78995 apa: Tomasek, K., Leithner, A. F., Glatzová, I., Lukesch, M. S., Guet, C. C., & Sixt, M. K. (2022). Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.78995 chicago: Tomasek, Kathrin, Alexander F Leithner, Ivana Glatzová, Michael S. Lukesch, Calin C Guet, and Michael K Sixt. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack the Host Immune Response by Binding to CD14.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/eLife.78995. ieee: K. Tomasek, A. F. Leithner, I. Glatzová, M. S. Lukesch, C. C. Guet, and M. K. Sixt, “Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14,” eLife, vol. 11. eLife Sciences Publications, 2022. ista: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. 2022. Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. eLife. 11, e78995. mla: Tomasek, Kathrin, et al. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack the Host Immune Response by Binding to CD14.” ELife, vol. 11, e78995, eLife Sciences Publications, 2022, doi:10.7554/eLife.78995. short: K. Tomasek, A.F. Leithner, I. Glatzová, M.S. Lukesch, C.C. Guet, M.K. Sixt, ELife 11 (2022). corr_author: '1' date_created: 2022-08-14T22:01:46Z date_published: 2022-07-26T00:00:00Z date_updated: 2025-04-15T07:17:32Z day: '26' ddc: - '570' department: - _id: MiSi - _id: CaGu doi: 10.7554/eLife.78995 ec_funded: 1 external_id: isi: - '000838410200001' pmid: - '35881547' file: - access_level: open_access checksum: 002a3c7c7ea5caa9af9cfbea308f6ea4 content_type: application/pdf creator: cchlebak date_created: 2022-08-16T08:57:37Z date_updated: 2022-08-16T08:57:37Z file_id: '11861' file_name: 2022_eLife_Tomasek.pdf file_size: 2057577 relation: main_file success: 1 file_date_updated: 2022-08-16T08:57:37Z has_accepted_license: '1' intvolume: ' 11' isi: 1 language: - iso: eng month: '07' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular Navigation Along Spatial Gradients - _id: 26018E70-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29911 name: Mechanical adaptation of lamellipodial actin publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' related_material: record: - id: '10316' relation: earlier_version status: public scopus_import: '1' status: public title: Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14 tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 11 year: '2022' ... --- _id: '12157' abstract: - lang: eng text: 'Polygenic adaptation is thought to be ubiquitous, yet remains poorly understood. Here, we model this process analytically, in the plausible setting of a highly polygenic, quantitative trait that experiences a sudden shift in the fitness optimum. We show how the mean phenotype changes over time, depending on the effect sizes of loci that contribute to variance in the trait, and characterize the allele dynamics at these loci. Notably, we describe the two phases of the allele dynamics: The first is a rapid phase, in which directional selection introduces small frequency differences between alleles whose effects are aligned with or opposed to the shift, ultimately leading to small differences in their probability of fixation during a second, longer phase, governed by stabilizing selection. As we discuss, key results should hold in more general settings and have important implications for efforts to identify the genetic basis of adaptation in humans and other species.' acknowledgement: "We thank Guy Amster, Jeremy Berg, Nick Barton, Yuval Simons and Molly Przeworski for many helpful discussions, and Jeremy Berg, Graham Coop, Joachim Hermisson, Guillaume Martin, Will Milligan, Peter Ralph, Yuval Simons, Leo Speidel and Molly Przeworski for comments on the manuscript.\r\nNational Institutes of Health GM115889 Laura Katharine Hayward Guy Sella \r\nNational Institutes of Health GM121372 Laura Katharine Hayward" article_number: '66697' article_processing_charge: No article_type: original author: - first_name: Laura full_name: Hayward, Laura id: fc885ee5-24bf-11eb-ad7b-bcc5104c0c1b last_name: Hayward - first_name: Guy full_name: Sella, Guy last_name: Sella citation: ama: Hayward L, Sella G. Polygenic adaptation after a sudden change in environment. eLife. 2022;11. doi:10.7554/elife.66697 apa: Hayward, L., & Sella, G. (2022). Polygenic adaptation after a sudden change in environment. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.66697 chicago: Hayward, Laura, and Guy Sella. “Polygenic Adaptation after a Sudden Change in Environment.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/elife.66697. ieee: L. Hayward and G. Sella, “Polygenic adaptation after a sudden change in environment,” eLife, vol. 11. eLife Sciences Publications, 2022. ista: Hayward L, Sella G. 2022. Polygenic adaptation after a sudden change in environment. eLife. 11, 66697. mla: Hayward, Laura, and Guy Sella. “Polygenic Adaptation after a Sudden Change in Environment.” ELife, vol. 11, 66697, eLife Sciences Publications, 2022, doi:10.7554/elife.66697. short: L. Hayward, G. Sella, ELife 11 (2022). corr_author: '1' date_created: 2023-01-12T12:09:00Z date_published: 2022-09-26T00:00:00Z date_updated: 2024-10-09T21:03:38Z day: '26' ddc: - '570' department: - _id: NiBa doi: 10.7554/elife.66697 external_id: isi: - '000890735600001' file: - access_level: open_access checksum: 28de155b231ac1c8d4501c98b2fb359a content_type: application/pdf creator: dernst date_created: 2023-01-24T12:21:32Z date_updated: 2023-01-24T12:21:32Z file_id: '12363' file_name: 2022_eLife_Hayward.pdf file_size: 18935612 relation: main_file success: 1 file_date_updated: 2023-01-24T12:21:32Z has_accepted_license: '1' intvolume: ' 11' isi: 1 keyword: - General Immunology and Microbiology - General Biochemistry - Genetics and Molecular Biology - General Medicine - General Neuroscience language: - iso: eng month: '09' oa: 1 oa_version: Published Version publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Polygenic adaptation after a sudden change in environment tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 11 year: '2022' ... --- _id: '12288' abstract: - lang: eng text: To understand the function of neuronal circuits, it is crucial to disentangle the connectivity patterns within the network. However, most tools currently used to explore connectivity have low throughput, low selectivity, or limited accessibility. Here, we report the development of an improved packaging system for the production of the highly neurotropic RVdGenvA-CVS-N2c rabies viral vectors, yielding titers orders of magnitude higher with no background contamination, at a fraction of the production time, while preserving the efficiency of transsynaptic labeling. Along with the production pipeline, we developed suites of ‘starter’ AAV and bicistronic RVdG-CVS-N2c vectors, enabling retrograde labeling from a wide range of neuronal populations, tailored for diverse experimental requirements. We demonstrate the power and flexibility of the new system by uncovering hidden local and distal inhibitory connections in the mouse hippocampal formation and by imaging the functional properties of a cortical microcircuit across weeks. Our novel production pipeline provides a convenient approach to generate new rabies vectors, while our toolkit flexibly and efficiently expands the current capacity to label, manipulate and image the neuronal activity of interconnected neuronal circuits in vitro and in vivo. acknowledged_ssus: - _id: Bio - _id: PreCl acknowledgement: We thank F Marr for technical assistance, A Murray for RVdG-CVS-N2c viruses and Neuro2A packaging cell-lines and J Watson for reading the manuscript. This research was supported by the Scientific Service Units (SSU) of IST-Austria through resources provided by the Imaging and Optics Facility (IOF) and the Preclinical Facility (PCF). This project was funded by the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (ERC advanced grant No 692692, PJ, ERC starting grant No 756502, MJ), the Fond zur Förderung der Wissenschaftlichen Forschung (Z 312-B27, Wittgenstein award, PJ), the Human Frontier Science Program (LT000256/2018-L, AS) and EMBO (ALTF 1098-2017, AS). article_number: '79848' article_processing_charge: No article_type: original author: - first_name: Anton L full_name: Sumser, Anton L id: 3320A096-F248-11E8-B48F-1D18A9856A87 last_name: Sumser orcid: 0000-0002-4792-1881 - first_name: Maximilian A full_name: Jösch, Maximilian A id: 2BD278E6-F248-11E8-B48F-1D18A9856A87 last_name: Jösch orcid: 0000-0002-3937-1330 - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: Yoav full_name: Ben Simon, Yoav id: 43DF3136-F248-11E8-B48F-1D18A9856A87 last_name: Ben Simon citation: ama: Sumser AL, Jösch MA, Jonas PM, Ben Simon Y. Fast, high-throughput production of improved rabies viral vectors for specific, efficient and versatile transsynaptic retrograde labeling. eLife. 2022;11. doi:10.7554/elife.79848 apa: Sumser, A. L., Jösch, M. A., Jonas, P. M., & Ben Simon, Y. (2022). Fast, high-throughput production of improved rabies viral vectors for specific, efficient and versatile transsynaptic retrograde labeling. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.79848 chicago: Sumser, Anton L, Maximilian A Jösch, Peter M Jonas, and Yoav Ben Simon. “Fast, High-Throughput Production of Improved Rabies Viral Vectors for Specific, Efficient and Versatile Transsynaptic Retrograde Labeling.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/elife.79848. ieee: A. L. Sumser, M. A. Jösch, P. M. Jonas, and Y. Ben Simon, “Fast, high-throughput production of improved rabies viral vectors for specific, efficient and versatile transsynaptic retrograde labeling,” eLife, vol. 11. eLife Sciences Publications, 2022. ista: Sumser AL, Jösch MA, Jonas PM, Ben Simon Y. 2022. Fast, high-throughput production of improved rabies viral vectors for specific, efficient and versatile transsynaptic retrograde labeling. eLife. 11, 79848. mla: Sumser, Anton L., et al. “Fast, High-Throughput Production of Improved Rabies Viral Vectors for Specific, Efficient and Versatile Transsynaptic Retrograde Labeling.” ELife, vol. 11, 79848, eLife Sciences Publications, 2022, doi:10.7554/elife.79848. short: A.L. Sumser, M.A. Jösch, P.M. Jonas, Y. Ben Simon, ELife 11 (2022). corr_author: '1' date_created: 2023-01-16T10:04:15Z date_published: 2022-09-15T00:00:00Z date_updated: 2025-04-15T08:29:05Z day: '15' ddc: - '570' department: - _id: MaJö - _id: PeJo doi: 10.7554/elife.79848 ec_funded: 1 external_id: isi: - '000892204300001' pmid: - '36040301' file: - access_level: open_access checksum: 5a2a65e3e7225090c3d8199f3bbd7b7b content_type: application/pdf creator: dernst date_created: 2023-01-30T11:50:53Z date_updated: 2023-01-30T11:50:53Z file_id: '12463' file_name: 2022_eLife_Sumser.pdf file_size: 8506811 relation: main_file success: 1 file_date_updated: 2023-01-30T11:50:53Z has_accepted_license: '1' intvolume: ' 11' isi: 1 keyword: - General Immunology and Microbiology - General Biochemistry - Genetics and Molecular Biology - General Medicine - General Neuroscience language: - iso: eng month: '09' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 25B7EB9E-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '692692' name: Biophysics and circuit function of a giant cortical glutamatergic synapse - _id: 2634E9D2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '756502' name: Circuits of Visual Attention - _id: 25C5A090-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Z00312 name: Synaptic communication in neuronal microcircuits - _id: 266D407A-B435-11E9-9278-68D0E5697425 grant_number: LT000256 name: Neuronal networks of salience and spatial detection in the murine superior colliculus - _id: 264FEA02-B435-11E9-9278-68D0E5697425 grant_number: ALTF 1098-2017 name: Connecting sensory with motor processing in the superior colliculus publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Fast, high-throughput production of improved rabies viral vectors for specific, efficient and versatile transsynaptic retrograde labeling tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 11 year: '2022' ... --- _id: '12333' abstract: - lang: eng text: Together, copy-number and point mutations form the basis for most evolutionary novelty, through the process of gene duplication and divergence. While a plethora of genomic data reveals the long-term fate of diverging coding sequences and their cis-regulatory elements, little is known about the early dynamics around the duplication event itself. In microorganisms, selection for increased gene expression often drives the expansion of gene copy-number mutations, which serves as a crude adaptation, prior to divergence through refining point mutations. Using a simple synthetic genetic reporter system that can distinguish between copy-number and point mutations, we study their early and transient adaptive dynamics in real time in Escherichia coli. We find two qualitatively different routes of adaptation, depending on the level of functional improvement needed. In conditions of high gene expression demand, the two mutation types occur as a combination. However, under low gene expression demand, copy-number and point mutations are mutually exclusive; here, owing to their higher frequency, adaptation is dominated by copy-number mutations, in a process we term amplification hindrance. Ultimately, due to high reversal rates and pleiotropic cost, copy-number mutations may not only serve as a crude and transient adaptation, but also constrain sequence divergence over evolutionary time scales. acknowledgement: "We are grateful to N Barton, F Kondrashov, M Lagator, M Pleska, R Roemhild, D Siekhaus, and G\r\nTkacik for input on the manuscript and to K Tomasek for help with flow cytometry." article_number: e82240 article_processing_charge: No article_type: original author: - first_name: Isabella full_name: Tomanek, Isabella id: 3981F020-F248-11E8-B48F-1D18A9856A87 last_name: Tomanek orcid: 0000-0001-6197-363X - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 citation: ama: Tomanek I, Guet CC. Adaptation dynamics between copynumber and point mutations. eLife. 2022;11. doi:10.7554/ELIFE.82240 apa: Tomanek, I., & Guet, C. C. (2022). Adaptation dynamics between copynumber and point mutations. ELife. eLife Sciences Publications. https://doi.org/10.7554/ELIFE.82240 chicago: Tomanek, Isabella, and Calin C Guet. “Adaptation Dynamics between Copynumber and Point Mutations.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/ELIFE.82240. ieee: I. Tomanek and C. C. Guet, “Adaptation dynamics between copynumber and point mutations,” eLife, vol. 11. eLife Sciences Publications, 2022. ista: Tomanek I, Guet CC. 2022. Adaptation dynamics between copynumber and point mutations. eLife. 11, e82240. mla: Tomanek, Isabella, and Calin C. Guet. “Adaptation Dynamics between Copynumber and Point Mutations.” ELife, vol. 11, e82240, eLife Sciences Publications, 2022, doi:10.7554/ELIFE.82240. short: I. Tomanek, C.C. Guet, ELife 11 (2022). corr_author: '1' date_created: 2023-01-22T23:00:55Z date_published: 2022-12-22T00:00:00Z date_updated: 2025-03-06T14:03:50Z day: '22' ddc: - '570' department: - _id: CaGu doi: 10.7554/ELIFE.82240 external_id: isi: - '000912674700001' pmid: - '36546673' file: - access_level: open_access checksum: 9321fd5f06ff59d5e2d33daee84b3da1 content_type: application/pdf creator: dernst date_created: 2023-01-23T08:56:21Z date_updated: 2023-01-23T08:56:21Z file_id: '12338' file_name: 2022_eLife_Tomanek.pdf file_size: 8835954 relation: main_file success: 1 file_date_updated: 2023-01-23T08:56:21Z has_accepted_license: '1' intvolume: ' 11' isi: 1 language: - iso: eng month: '12' oa: 1 oa_version: Published Version pmid: 1 publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' related_material: link: - relation: software url: https://doi.org/10.5281/zenodo.6974122 record: - id: '12339' relation: research_data status: public scopus_import: '1' status: public title: Adaptation dynamics between copynumber and point mutations tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 11 year: '2022' ... --- _id: '10736' abstract: - lang: eng text: Predicting function from sequence is a central problem of biology. Currently, this is possible only locally in a narrow mutational neighborhood around a wildtype sequence rather than globally from any sequence. Using random mutant libraries, we developed a biophysical model that accounts for multiple features of σ70 binding bacterial promoters to predict constitutive gene expression levels from any sequence. We experimentally and theoretically estimated that 10–20% of random sequences lead to expression and ~80% of non-expressing sequences are one mutation away from a functional promoter. The potential for generating expression from random sequences is so pervasive that selection acts against σ70-RNA polymerase binding sites even within inter-genic, promoter-containing regions. This pervasiveness of σ70-binding sites implies that emergence of promoters is not the limiting step in gene regulatory evolution. Ultimately, the inclusion of novel features of promoter function into a mechanistic model enabled not only more accurate predictions of gene expression levels, but also identified that promoters evolve more rapidly than previously thought. acknowledgement: 'We thank Hande Acar, Nicholas H Barton, Rok Grah, Tiago Paixao, Maros Pleska, Anna Staron, and Murat Tugrul for insightful comments and input on the manuscript. This work was supported by: Sir Henry Dale Fellowship jointly funded by the Wellcome Trust and the Royal Society (grant number 216779/Z/19/Z) to ML; IPC Grant from IST Austria to ML and SS; European Research Council Funding Programme 7 (2007–2013, grant agreement number 648440) to JPB.' article_number: e64543 article_processing_charge: No article_type: original author: - first_name: Mato full_name: Lagator, Mato id: 345D25EC-F248-11E8-B48F-1D18A9856A87 last_name: Lagator - first_name: Srdjan full_name: Sarikas, Srdjan id: 35F0286E-F248-11E8-B48F-1D18A9856A87 last_name: Sarikas - first_name: Magdalena full_name: Steinrück, Magdalena id: 2C023F40-F248-11E8-B48F-1D18A9856A87 last_name: Steinrück orcid: 0000-0003-1229-9719 - first_name: David full_name: Toledo-Aparicio, David last_name: Toledo-Aparicio - first_name: Jonathan P full_name: Bollback, Jonathan P id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87 last_name: Bollback orcid: 0000-0002-4624-4612 - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 - first_name: Gašper full_name: Tkačik, Gašper id: 3D494DCA-F248-11E8-B48F-1D18A9856A87 last_name: Tkačik orcid: 0000-0002-6699-1455 citation: ama: Lagator M, Sarikas S, Steinrück M, et al. Predicting bacterial promoter function and evolution from random sequences. eLife. 2022;11. doi:10.7554/eLife.64543 apa: Lagator, M., Sarikas, S., Steinrück, M., Toledo-Aparicio, D., Bollback, J. P., Guet, C. C., & Tkačik, G. (2022). Predicting bacterial promoter function and evolution from random sequences. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.64543 chicago: Lagator, Mato, Srdjan Sarikas, Magdalena Steinrück, David Toledo-Aparicio, Jonathan P Bollback, Calin C Guet, and Gašper Tkačik. “Predicting Bacterial Promoter Function and Evolution from Random Sequences.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/eLife.64543. ieee: M. Lagator et al., “Predicting bacterial promoter function and evolution from random sequences,” eLife, vol. 11. eLife Sciences Publications, 2022. ista: Lagator M, Sarikas S, Steinrück M, Toledo-Aparicio D, Bollback JP, Guet CC, Tkačik G. 2022. Predicting bacterial promoter function and evolution from random sequences. eLife. 11, e64543. mla: Lagator, Mato, et al. “Predicting Bacterial Promoter Function and Evolution from Random Sequences.” ELife, vol. 11, e64543, eLife Sciences Publications, 2022, doi:10.7554/eLife.64543. short: M. Lagator, S. Sarikas, M. Steinrück, D. Toledo-Aparicio, J.P. Bollback, C.C. Guet, G. Tkačik, ELife 11 (2022). corr_author: '1' date_created: 2022-02-06T23:01:32Z date_published: 2022-01-26T00:00:00Z date_updated: 2025-03-31T16:00:23Z day: '26' ddc: - '576' department: - _id: CaGu - _id: GaTk - _id: NiBa doi: 10.7554/eLife.64543 ec_funded: 1 external_id: isi: - '000751104400001' pmid: - '35080492' file: - access_level: open_access checksum: decdcdf600ff51e9a9703b49ca114170 content_type: application/pdf creator: cchlebak date_created: 2022-02-07T07:14:09Z date_updated: 2022-02-07T07:14:09Z file_id: '10739' file_name: 2022_ELife_Lagator.pdf file_size: 5604343 relation: main_file success: 1 file_date_updated: 2022-02-07T07:14:09Z has_accepted_license: '1' intvolume: ' 11' isi: 1 language: - iso: eng month: '01' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 2578D616-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '648440' name: Selective Barriers to Horizontal Gene Transfer publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Predicting bacterial promoter function and evolution from random sequences tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 11 year: '2022' ... --- _id: '11419' abstract: - lang: eng text: Elevation of soluble wild-type (WT) tau occurs in synaptic compartments in Alzheimer’s disease. We addressed whether tau elevation affects synaptic transmission at the calyx of Held in slices from mice brainstem. Whole-cell loading of WT human tau (h-tau) in presynaptic terminals at 10–20 µM caused microtubule (MT) assembly and activity-dependent rundown of excitatory neurotransmission. Capacitance measurements revealed that the primary target of WT h-tau is vesicle endocytosis. Blocking MT assembly using nocodazole prevented tau-induced impairments of endocytosis and neurotransmission. Immunofluorescence imaging analyses revealed that MT assembly by WT h-tau loading was associated with an increased MT-bound fraction of the endocytic protein dynamin. A synthetic dodecapeptide corresponding to dynamin 1-pleckstrin-homology domain inhibited MT-dynamin interaction and rescued tau-induced impairments of endocytosis and neurotransmission. We conclude that elevation of presynaptic WT tau induces de novo assembly of MTs, thereby sequestering free dynamins. As a result, endocytosis and subsequent vesicle replenishment are impaired, causing activity-dependent rundown of neurotransmission. acknowledgement: We thank Yasuo Ihara, Nobuyuki Nukina, and Takeshi Sakaba for comments and Patrick Stoney for editing this paper. We also thank Shota Okuda and Mikako Matsubara for their contributions in the early stage of this study, and Satoko Wada-Kakuda for technical assistant with in vitro analysis of tau. This research was supported by funding from Okinawa Institute of Science and Technology and from Technology (OIST) and Core Research for the Evolutional Science and Technology of Japan Science and Technology Agency (CREST) to TT, and by Scientific Research on Innovative Areas to TM (Brain Protein Aging and Dementia Control 26117004). article_number: e73542 article_processing_charge: No article_type: original author: - first_name: Tetsuya full_name: Hori, Tetsuya last_name: Hori - first_name: Kohgaku full_name: Eguchi, Kohgaku id: 2B7846DC-F248-11E8-B48F-1D18A9856A87 last_name: Eguchi orcid: 0000-0002-6170-2546 - first_name: Han Ying full_name: Wang, Han Ying last_name: Wang - first_name: Tomohiro full_name: Miyasaka, Tomohiro last_name: Miyasaka - first_name: Laurent full_name: Guillaud, Laurent last_name: Guillaud - first_name: Zacharie full_name: Taoufiq, Zacharie last_name: Taoufiq - first_name: Satyajit full_name: Mahapatra, Satyajit last_name: Mahapatra - first_name: Hiroshi full_name: Yamada, Hiroshi last_name: Yamada - first_name: Kohji full_name: Takei, Kohji last_name: Takei - first_name: Tomoyuki full_name: Takahashi, Tomoyuki last_name: Takahashi citation: ama: Hori T, Eguchi K, Wang HY, et al. Microtubule assembly by tau impairs endocytosis and neurotransmission via dynamin sequestration in Alzheimer’s disease synapse model. eLife. 2022;11. doi:10.7554/eLife.73542 apa: Hori, T., Eguchi, K., Wang, H. Y., Miyasaka, T., Guillaud, L., Taoufiq, Z., … Takahashi, T. (2022). Microtubule assembly by tau impairs endocytosis and neurotransmission via dynamin sequestration in Alzheimer’s disease synapse model. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.73542 chicago: Hori, Tetsuya, Kohgaku Eguchi, Han Ying Wang, Tomohiro Miyasaka, Laurent Guillaud, Zacharie Taoufiq, Satyajit Mahapatra, Hiroshi Yamada, Kohji Takei, and Tomoyuki Takahashi. “Microtubule Assembly by Tau Impairs Endocytosis and Neurotransmission via Dynamin Sequestration in Alzheimer’s Disease Synapse Model.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/eLife.73542. ieee: T. Hori et al., “Microtubule assembly by tau impairs endocytosis and neurotransmission via dynamin sequestration in Alzheimer’s disease synapse model,” eLife, vol. 11. eLife Sciences Publications, 2022. ista: Hori T, Eguchi K, Wang HY, Miyasaka T, Guillaud L, Taoufiq Z, Mahapatra S, Yamada H, Takei K, Takahashi T. 2022. Microtubule assembly by tau impairs endocytosis and neurotransmission via dynamin sequestration in Alzheimer’s disease synapse model. eLife. 11, e73542. mla: Hori, Tetsuya, et al. “Microtubule Assembly by Tau Impairs Endocytosis and Neurotransmission via Dynamin Sequestration in Alzheimer’s Disease Synapse Model.” ELife, vol. 11, e73542, eLife Sciences Publications, 2022, doi:10.7554/eLife.73542. short: T. Hori, K. Eguchi, H.Y. Wang, T. Miyasaka, L. Guillaud, Z. Taoufiq, S. Mahapatra, H. Yamada, K. Takei, T. Takahashi, ELife 11 (2022). date_created: 2022-05-29T22:01:54Z date_published: 2022-05-05T00:00:00Z date_updated: 2023-08-03T07:15:49Z day: '05' ddc: - '616' department: - _id: RySh doi: 10.7554/eLife.73542 external_id: isi: - '000876231600001' pmid: - '35471147 ' file: - access_level: open_access checksum: ccddbd167e00ff8375f12998af497152 content_type: application/pdf creator: cchlebak date_created: 2022-05-30T08:09:16Z date_updated: 2022-05-30T08:09:16Z file_id: '11421' file_name: elife-73542-v2.pdf file_size: 2466296 relation: main_file success: 1 file_date_updated: 2022-05-30T08:09:16Z has_accepted_license: '1' intvolume: ' 11' isi: 1 language: - iso: eng month: '05' oa: 1 oa_version: Published Version pmid: 1 publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Microtubule assembly by tau impairs endocytosis and neurotransmission via dynamin sequestration in Alzheimer's disease synapse model tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 11 year: '2022' ... --- _id: '10826' abstract: - lang: eng text: Animals that lose one sensory modality often show augmented responses to other sensory inputs. The mechanisms underpinning this cross-modal plasticity are poorly understood. We probe such mechanisms by performing a forward genetic screen for mutants with enhanced O2 perception in Caenorhabditis elegans. Multiple mutants exhibiting increased O2 responsiveness concomitantly show defects in other sensory responses. One mutant, qui-1, defective in a conserved NACHT/WD40 protein, abolishes pheromone-evoked Ca2+ responses in the ADL pheromone-sensing neurons. At the same time, ADL responsiveness to pre-synaptic input from O2-sensing neurons is heightened in qui-1, and other sensory defective mutants, resulting in enhanced neurosecretion although not increased Ca2+ responses. Expressing qui-1 selectively in ADL rescues both the qui-1 ADL neurosecretory phenotype and enhanced escape from 21% O2. Profiling ADL neurons in qui-1 mutants highlights extensive changes in gene expression, notably of many neuropeptide receptors. We show that elevated ADL expression of the conserved neuropeptide receptor NPR-22 is necessary for enhanced ADL neurosecretion in qui-1 mutants, and is sufficient to confer increased ADL neurosecretion in control animals. Sensory loss can thus confer cross-modal plasticity by changing the peptidergic connectome. acknowledged_ssus: - _id: Bio - _id: LifeSc - _id: ScienComp acknowledgement: "We would like to thank Gemma Chandratillake and Merav Cohen for identifying mutants and José David Moñino Sánchez for his help on neurosecretion assays. We are grateful to Kaveh Ashrafi (UCSF), Piali Sengupta (Brandeis), and the Caenorhabditis Genetic Center (funded by National Institutes of Health Infrastructure Program P40 OD010440) for strains and reagents ... and Rebecca Butcher (Univ. Florida) for C9 pheromone. We thank Tim Stevens, Paula Freire-Pritchett, Alastair Crisp, GurpreetGhattaoraya, and Fabian Amman for help with bioinformatic analysis, Ekaterina Lashmanova for help with injections, Iris Hardege for strains, and Isabel Beets (KU Leuven) and members of the de Bono Lab for comments on the manuscript. We thank the CRUK Cambridge Research Institute Genomics Core for next generation sequencing and the Flow Cytometry Facility at LMB for FACS. This research was supported by the Scientific Service Units (SSU) of IST Austria through resources provided by the Bioimaging Facility (BIF), the Life Science Facility (LSF) and Scientific Computing (SciCo-p– Bioinformatics).\r\nThis work was supported by the Medical Research Council UK (Studentship to GV), an\r\nAdvanced ERC grant (269,058 ACMO to MdB), and a Wellcome Investigator Award (209504/Z/17/Z to MdB)." article_number: e68040 article_processing_charge: No article_type: original author: - first_name: Giulio full_name: Valperga, Giulio id: 67F289DE-0D8F-11EA-9BDD-54AE3DDC885E last_name: Valperga orcid: 0000-0001-6726-3890 - first_name: Mario full_name: De Bono, Mario id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87 last_name: De Bono orcid: 0000-0001-8347-0443 citation: ama: Valperga G, de Bono M. Impairing one sensory modality enhances another by reconfiguring peptidergic signalling in Caenorhabditis elegans. eLife. 2022;11. doi:10.7554/eLife.68040 apa: Valperga, G., & de Bono, M. (2022). Impairing one sensory modality enhances another by reconfiguring peptidergic signalling in Caenorhabditis elegans. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.68040 chicago: Valperga, Giulio, and Mario de Bono. “Impairing One Sensory Modality Enhances Another by Reconfiguring Peptidergic Signalling in Caenorhabditis Elegans.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/eLife.68040. ieee: G. Valperga and M. de Bono, “Impairing one sensory modality enhances another by reconfiguring peptidergic signalling in Caenorhabditis elegans,” eLife, vol. 11. eLife Sciences Publications, 2022. ista: Valperga G, de Bono M. 2022. Impairing one sensory modality enhances another by reconfiguring peptidergic signalling in Caenorhabditis elegans. eLife. 11, e68040. mla: Valperga, Giulio, and Mario de Bono. “Impairing One Sensory Modality Enhances Another by Reconfiguring Peptidergic Signalling in Caenorhabditis Elegans.” ELife, vol. 11, e68040, eLife Sciences Publications, 2022, doi:10.7554/eLife.68040. short: G. Valperga, M. de Bono, ELife 11 (2022). corr_author: '1' date_created: 2022-03-06T23:01:52Z date_published: 2022-02-24T00:00:00Z date_updated: 2026-04-02T12:45:39Z day: '24' ddc: - '570' department: - _id: MaDe doi: 10.7554/eLife.68040 external_id: isi: - '000763432300001' pmid: - '35201977' file: - access_level: open_access checksum: cc1b9bf866d0f61f965556e0dd03d3ac content_type: application/pdf creator: dernst date_created: 2022-03-07T07:39:25Z date_updated: 2022-03-07T07:39:25Z file_id: '10830' file_name: 2022_eLife_Valperga.pdf file_size: 4095591 relation: main_file success: 1 file_date_updated: 2022-03-07T07:39:25Z has_accepted_license: '1' intvolume: ' 11' isi: 1 language: - iso: eng month: '02' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 23870BE8-32DE-11EA-91FC-C7463DDC885E grant_number: 209504/A/17/Z name: Molecular mechanisms of neural circuit function publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Impairing one sensory modality enhances another by reconfiguring peptidergic signalling in Caenorhabditis elegans tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd volume: 11 year: '2022' ... --- DOAJ_listed: '1' OA_place: publisher OA_type: gold _id: '19472' abstract: - lang: eng text: The forebrain hemispheres are predominantly separated during embryogenesis by the interhemispheric fissure (IHF). Radial astroglia remodel the IHF to form a continuous substrate between the hemispheres for midline crossing of the corpus callosum (CC) and hippocampal commissure (HC). Deleted in colorectal carcinoma (DCC) and netrin 1 (NTN1) are molecules that have an evolutionarily conserved function in commissural axon guidance. The CC and HC are absent in Dcc and Ntn1 knockout mice, while other commissures are only partially affected, suggesting an additional aetiology in forebrain commissure formation. Here, we find that these molecules play a critical role in regulating astroglial development and IHF remodelling during CC and HC formation. Human subjects with DCC mutations display disrupted IHF remodelling associated with CC and HC malformations. Thus, axon guidance molecules such as DCC and NTN1 first regulate the formation of a midline substrate for dorsal commissures prior to their role in regulating axonal growth and guidance across it. article_number: '61769' article_processing_charge: Yes article_type: original author: - first_name: Laura full_name: Morcom, Laura last_name: Morcom - first_name: Ilan full_name: Gobius, Ilan last_name: Gobius - first_name: Ashley PL full_name: Marsh, Ashley PL last_name: Marsh - first_name: Rodrigo full_name: Suárez, Rodrigo last_name: Suárez - first_name: Jonathan WC full_name: Lim, Jonathan WC last_name: Lim - first_name: Caitlin full_name: Bridges, Caitlin last_name: Bridges - first_name: Yunan full_name: Ye, Yunan last_name: Ye - first_name: Laura R full_name: Fenlon, Laura R last_name: Fenlon - first_name: Yvrick full_name: Zagar, Yvrick last_name: Zagar - first_name: Amelia May Barnett full_name: Douglass, Amelia May Barnett id: de5f6fda-80fb-11ef-996f-a8c4ecd8e289 last_name: Douglass orcid: 0000-0001-5398-6473 - first_name: Amber-Lee S full_name: Donahoo, Amber-Lee S last_name: Donahoo - first_name: Thomas full_name: Fothergill, Thomas last_name: Fothergill - first_name: Samreen full_name: Shaikh, Samreen last_name: Shaikh - first_name: Peter full_name: Kozulin, Peter last_name: Kozulin - first_name: Timothy J full_name: Edwards, Timothy J last_name: Edwards - first_name: Helen M full_name: Cooper, Helen M last_name: Cooper - first_name: Elliott H full_name: Sherr, Elliott H last_name: Sherr - first_name: Alain full_name: Chédotal, Alain last_name: Chédotal - first_name: Richard J full_name: Leventer, Richard J last_name: Leventer - first_name: Paul J full_name: Lockhart, Paul J last_name: Lockhart - first_name: Linda J full_name: Richards, Linda J last_name: Richards citation: ama: Morcom L, Gobius I, Marsh AP, et al. DCC regulates astroglial development essential for telencephalic morphogenesis and corpus callosum formation. eLife. 2021;10. doi:10.7554/elife.61769 apa: Morcom, L., Gobius, I., Marsh, A. P., Suárez, R., Lim, J. W., Bridges, C., … Richards, L. J. (2021). DCC regulates astroglial development essential for telencephalic morphogenesis and corpus callosum formation. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.61769 chicago: Morcom, Laura, Ilan Gobius, Ashley PL Marsh, Rodrigo Suárez, Jonathan WC Lim, Caitlin Bridges, Yunan Ye, et al. “DCC Regulates Astroglial Development Essential for Telencephalic Morphogenesis and Corpus Callosum Formation.” ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/elife.61769. ieee: L. Morcom et al., “DCC regulates astroglial development essential for telencephalic morphogenesis and corpus callosum formation,” eLife, vol. 10. eLife Sciences Publications, 2021. ista: Morcom L, Gobius I, Marsh AP, Suárez R, Lim JW, Bridges C, Ye Y, Fenlon LR, Zagar Y, Douglass AM, Donahoo A-LS, Fothergill T, Shaikh S, Kozulin P, Edwards TJ, Cooper HM, Sherr EH, Chédotal A, Leventer RJ, Lockhart PJ, Richards LJ. 2021. DCC regulates astroglial development essential for telencephalic morphogenesis and corpus callosum formation. eLife. 10, 61769. mla: Morcom, Laura, et al. “DCC Regulates Astroglial Development Essential for Telencephalic Morphogenesis and Corpus Callosum Formation.” ELife, vol. 10, 61769, eLife Sciences Publications, 2021, doi:10.7554/elife.61769. short: L. Morcom, I. Gobius, A.P. Marsh, R. Suárez, J.W. Lim, C. Bridges, Y. Ye, L.R. Fenlon, Y. Zagar, A.M. Douglass, A.-L.S. Donahoo, T. Fothergill, S. Shaikh, P. Kozulin, T.J. Edwards, H.M. Cooper, E.H. Sherr, A. Chédotal, R.J. Leventer, P.J. Lockhart, L.J. Richards, ELife 10 (2021). date_created: 2025-04-03T12:29:29Z date_published: 2021-04-19T00:00:00Z date_updated: 2025-07-10T11:51:41Z day: '19' doi: 10.7554/elife.61769 extern: '1' external_id: pmid: - '33871356' has_accepted_license: '1' intvolume: ' 10' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.7554/eLife.61769 month: '04' oa: 1 oa_version: Published Version pmid: 1 publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: DCC regulates astroglial development essential for telencephalic morphogenesis and corpus callosum formation tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 10 year: '2021' ... --- _id: '10606' abstract: - lang: eng text: Cell division orientation is thought to result from a competition between cell geometry and polarity domains controlling the position of the mitotic spindle during mitosis. Depending on the level of cell shape anisotropy or the strength of the polarity domain, one dominates the other and determines the orientation of the spindle. Whether and how such competition is also at work to determine unequal cell division (UCD), producing daughter cells of different size, remains unclear. Here, we show that cell geometry and polarity domains cooperate, rather than compete, in positioning the cleavage plane during UCDs in early ascidian embryos. We found that the UCDs and their orientation at the ascidian third cleavage rely on the spindle tilting in an anisotropic cell shape, and cortical polarity domains exerting different effects on spindle astral microtubules. By systematically varying mitotic cell shape, we could modulate the effect of attractive and repulsive polarity domains and consequently generate predicted daughter cell size asymmetries and position. We therefore propose that the spindle position during UCD is set by the combined activities of cell geometry and polarity domains, where cell geometry modulates the effect of cortical polarity domain(s). acknowledged_ssus: - _id: NanoFab - _id: Bio acknowledgement: 'We thank members of the Heisenberg and McDougall groups for technical advice and discussion. We are grateful to the Bioimaging and Nanofabrication facilities of IST Austria and the Imaging Platform (PIM) and animal facility (CRB) of Institut de la Mer de Villefranche (IMEV), which is supported by EMBRC-France, whose French state funds are managed by the ANR within the Investments of the Future program under reference ANR-10-INBS-0, for continuous support. This work was supported by a collaborative grant from the French Government funding agency Agence National de la Recherche to McDougall (ANR ''MorCell'': ANR-17-CE 13-0028) and the Austrian Science Fund to Heisenberg (FWF: I 3601-B27).' article_number: e75639 article_processing_charge: No article_type: original author: - first_name: Benoit G full_name: Godard, Benoit G id: 33280250-F248-11E8-B48F-1D18A9856A87 last_name: Godard - first_name: Remi full_name: Dumollard, Remi last_name: Dumollard - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 - first_name: Alex full_name: Mcdougall, Alex last_name: Mcdougall citation: ama: Godard BG, Dumollard R, Heisenberg C-PJ, Mcdougall A. Combined effect of cell geometry and polarity domains determines the orientation of unequal division. eLife. 2021;10. doi:10.7554/eLife.75639 apa: Godard, B. G., Dumollard, R., Heisenberg, C.-P. J., & Mcdougall, A. (2021). Combined effect of cell geometry and polarity domains determines the orientation of unequal division. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.75639 chicago: Godard, Benoit G, Remi Dumollard, Carl-Philipp J Heisenberg, and Alex Mcdougall. “Combined Effect of Cell Geometry and Polarity Domains Determines the Orientation of Unequal Division.” ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/eLife.75639. ieee: B. G. Godard, R. Dumollard, C.-P. J. Heisenberg, and A. Mcdougall, “Combined effect of cell geometry and polarity domains determines the orientation of unequal division,” eLife, vol. 10. eLife Sciences Publications, 2021. ista: Godard BG, Dumollard R, Heisenberg C-PJ, Mcdougall A. 2021. Combined effect of cell geometry and polarity domains determines the orientation of unequal division. eLife. 10, e75639. mla: Godard, Benoit G., et al. “Combined Effect of Cell Geometry and Polarity Domains Determines the Orientation of Unequal Division.” ELife, vol. 10, e75639, eLife Sciences Publications, 2021, doi:10.7554/eLife.75639. short: B.G. Godard, R. Dumollard, C.-P.J. Heisenberg, A. Mcdougall, ELife 10 (2021). corr_author: '1' date_created: 2022-01-09T23:01:26Z date_published: 2021-12-21T00:00:00Z date_updated: 2025-04-14T12:59:47Z day: '21' ddc: - '570' department: - _id: CaHe doi: 10.7554/eLife.75639 external_id: isi: - '000733610100001' pmid: - '34889186' file: - access_level: open_access checksum: 759c7a873d554c48a6639e6350746ca6 content_type: application/pdf creator: alisjak date_created: 2022-01-10T09:40:37Z date_updated: 2022-01-10T09:40:37Z file_id: '10611' file_name: 2021_eLife_Godard.pdf file_size: 7769934 relation: main_file success: 1 file_date_updated: 2022-01-10T09:40:37Z has_accepted_license: '1' intvolume: ' 10' isi: 1 language: - iso: eng month: '12' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 2646861A-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: I03601 name: Control of embryonic cleavage pattern publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Combined effect of cell geometry and polarity domains determines the orientation of unequal division tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 10 year: '2021' ... --- _id: '10116' abstract: - lang: eng text: The ubiquitous Ca2+ sensor calmodulin (CaM) binds and regulates many proteins, including ion channels, CaM kinases, and calcineurin, according to Ca2+-CaM levels. What regulates neuronal CaM levels, is, however, unclear. CaM-binding transcription activators (CAMTAs) are ancient proteins expressed broadly in nervous systems and whose loss confers pleiotropic behavioral defects in flies, mice, and humans. Using Caenorhabditis elegans and Drosophila, we show that CAMTAs control neuronal CaM levels. The behavioral and neuronal Ca2+ signaling defects in mutants lacking camt-1, the sole C. elegans CAMTA, can be rescued by supplementing neuronal CaM. CAMT-1 binds multiple sites in the CaM promoter and deleting these sites phenocopies camt-1. Our data suggest CAMTAs mediate a conserved and general mechanism that controls neuronal CaM levels, thereby regulating Ca2+ signaling, physiology, and behavior. acknowledgement: The authors thank the MRC-LMB Flow Cytometry facility and Imaging Service for support, the Cancer Research UK Cambridge Institute Genomics Core for Next Generation Sequencing, Julie Ahringer and Alex Appert for advice and technical help for ChIP-seq experiments, Paula Freire-Pritchett, Tim Stevens, and Gurpreet Ghattaoraya for RNA-seq and ChIP-seq analyses, Nikos Chronis for the TN-XL plasmid, Hong-Sheng Li and Daisuke Yamamoto for generously sending the tes2 and cro mutants, Daria Siekhaus for hosting the fly work, Michaela Misova for technical assistance. The authors are very grateful to Salihah Ece Sönmez for teaching us how to dissect, mount and stain Drosophila retinae. This work was supported by an Advanced ERC grant (269058 ACMO) and a Wellcome Investigator Award (209504/Z/17/Z) to MdB, and an IST Plus Fellowship to TV-B (Marie Sklodowska-Curie Agreement no 754411). article_number: e68238 article_processing_charge: No article_type: original author: - first_name: Thanh full_name: Vuong-Brender, Thanh id: D389312E-10C4-11EA-ABF4-A4B43DDC885E last_name: Vuong-Brender - first_name: Sean full_name: Flynn, Sean last_name: Flynn - first_name: Yvonne full_name: Vallis, Yvonne id: 05A2795C-31B5-11EA-83A7-7DA23DDC885E last_name: Vallis - first_name: Mario full_name: De Bono, Mario id: 4E3FF80E-F248-11E8-B48F-1D18A9856A87 last_name: De Bono orcid: 0000-0001-8347-0443 citation: ama: Vuong-Brender T, Flynn S, Vallis Y, de Bono M. Neuronal calmodulin levels are controlled by CAMTA transcription factors. eLife. 2021;10. doi:10.7554/eLife.68238 apa: Vuong-Brender, T., Flynn, S., Vallis, Y., & de Bono, M. (2021). Neuronal calmodulin levels are controlled by CAMTA transcription factors. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.68238 chicago: Vuong-Brender, Thanh, Sean Flynn, Yvonne Vallis, and Mario de Bono. “Neuronal Calmodulin Levels Are Controlled by CAMTA Transcription Factors.” ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/eLife.68238. ieee: T. Vuong-Brender, S. Flynn, Y. Vallis, and M. de Bono, “Neuronal calmodulin levels are controlled by CAMTA transcription factors,” eLife, vol. 10. eLife Sciences Publications, 2021. ista: Vuong-Brender T, Flynn S, Vallis Y, de Bono M. 2021. Neuronal calmodulin levels are controlled by CAMTA transcription factors. eLife. 10, e68238. mla: Vuong-Brender, Thanh, et al. “Neuronal Calmodulin Levels Are Controlled by CAMTA Transcription Factors.” ELife, vol. 10, e68238, eLife Sciences Publications, 2021, doi:10.7554/eLife.68238. short: T. Vuong-Brender, S. Flynn, Y. Vallis, M. de Bono, ELife 10 (2021). date_created: 2021-10-10T22:01:22Z date_published: 2021-09-17T00:00:00Z date_updated: 2025-04-14T07:43:46Z day: '17' ddc: - '610' department: - _id: MaDe doi: 10.7554/eLife.68238 ec_funded: 1 external_id: isi: - '000695716100001' pmid: - '34499028' file: - access_level: open_access checksum: b465e172d2b1f57aa26a2571a085d052 content_type: application/pdf creator: cchlebak date_created: 2021-10-11T14:15:07Z date_updated: 2021-10-11T14:15:07Z file_id: '10122' file_name: 2021_eLife_VuongBrender.pdf file_size: 1774624 relation: main_file success: 1 file_date_updated: 2021-10-11T14:15:07Z has_accepted_license: '1' intvolume: ' 10' isi: 1 language: - iso: eng month: '09' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 260C2330-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '754411' name: ISTplus - Postdoctoral Fellowships publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Neuronal calmodulin levels are controlled by CAMTA transcription factors tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 10 year: '2021' ... --- _id: '10403' abstract: - lang: eng text: Synaptic transmission, connectivity, and dendritic morphology mature in parallel during brain development and are often disrupted in neurodevelopmental disorders. Yet how these changes influence the neuronal computations necessary for normal brain function are not well understood. To identify cellular mechanisms underlying the maturation of synaptic integration in interneurons, we combined patch-clamp recordings of excitatory inputs in mouse cerebellar stellate cells (SCs), three-dimensional reconstruction of SC morphology with excitatory synapse location, and biophysical modeling. We found that postnatal maturation of postsynaptic strength was homogeneously reduced along the somatodendritic axis, but dendritic integration was always sublinear. However, dendritic branching increased without changes in synapse density, leading to a substantial gain in distal inputs. Thus, changes in synapse distribution, rather than dendrite cable properties, are the dominant mechanism underlying the maturation of neuronal computation. These mechanisms favor the emergence of a spatially compartmentalized two-stage integration model promoting location-dependent integration within dendritic subunits. acknowledgement: This study was supported by the Centre National de la Recherche Scientifique and the Agence Nationale de la Recherche (ANR-13-BSV4-00166, to LC and DAD). TA was supported by fellowships from the Fondation pour la Recherche Medicale and the Swedish Research Council. We thank Dmitry Ershov from the Image Analysis Hub of the Institut Pasteur, Elodie Le Monnier, Elena Hollergschwandtner, Vanessa Zheden, and Corinne Nantet for technical support and Haining Zhong for providing the Venus-tagged PSD95 mouse line. We would like to thank Alberto Bacci, Ann Lohof, and Nelson Rebola for comments on the manuscript. article_number: e65954 article_processing_charge: No article_type: original author: - first_name: Celia full_name: Biane, Celia last_name: Biane - first_name: Florian full_name: Rückerl, Florian last_name: Rückerl - first_name: Therese full_name: Abrahamsson, Therese last_name: Abrahamsson - first_name: Cécile full_name: Saint-Cloment, Cécile last_name: Saint-Cloment - first_name: Jean full_name: Mariani, Jean last_name: Mariani - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: David A. full_name: Digregorio, David A. last_name: Digregorio - first_name: Rachel M. full_name: Sherrard, Rachel M. last_name: Sherrard - first_name: Laurence full_name: Cathala, Laurence last_name: Cathala citation: ama: Biane C, Rückerl F, Abrahamsson T, et al. Developmental emergence of two-stage nonlinear synaptic integration in cerebellar interneurons. eLife. 2021;10. doi:10.7554/eLife.65954 apa: Biane, C., Rückerl, F., Abrahamsson, T., Saint-Cloment, C., Mariani, J., Shigemoto, R., … Cathala, L. (2021). Developmental emergence of two-stage nonlinear synaptic integration in cerebellar interneurons. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.65954 chicago: Biane, Celia, Florian Rückerl, Therese Abrahamsson, Cécile Saint-Cloment, Jean Mariani, Ryuichi Shigemoto, David A. Digregorio, Rachel M. Sherrard, and Laurence Cathala. “Developmental Emergence of Two-Stage Nonlinear Synaptic Integration in Cerebellar Interneurons.” ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/eLife.65954. ieee: C. Biane et al., “Developmental emergence of two-stage nonlinear synaptic integration in cerebellar interneurons,” eLife, vol. 10. eLife Sciences Publications, 2021. ista: Biane C, Rückerl F, Abrahamsson T, Saint-Cloment C, Mariani J, Shigemoto R, Digregorio DA, Sherrard RM, Cathala L. 2021. Developmental emergence of two-stage nonlinear synaptic integration in cerebellar interneurons. eLife. 10, e65954. mla: Biane, Celia, et al. “Developmental Emergence of Two-Stage Nonlinear Synaptic Integration in Cerebellar Interneurons.” ELife, vol. 10, e65954, eLife Sciences Publications, 2021, doi:10.7554/eLife.65954. short: C. Biane, F. Rückerl, T. Abrahamsson, C. Saint-Cloment, J. Mariani, R. Shigemoto, D.A. Digregorio, R.M. Sherrard, L. Cathala, ELife 10 (2021). date_created: 2021-12-05T23:01:40Z date_published: 2021-11-03T00:00:00Z date_updated: 2025-03-07T08:12:39Z day: '03' ddc: - '570' department: - _id: RySh doi: 10.7554/eLife.65954 external_id: isi: - '000715789500001' pmid: - '34730085' file: - access_level: open_access checksum: c7c33c3319428d56e332e22349c50ed3 content_type: application/pdf creator: cchlebak date_created: 2021-12-10T08:31:41Z date_updated: 2021-12-10T08:31:41Z file_id: '10528' file_name: 2021_eLife_Biane.pdf file_size: 13131322 relation: main_file success: 1 file_date_updated: 2021-12-10T08:31:41Z has_accepted_license: '1' intvolume: ' 10' isi: 1 language: - iso: eng month: '11' oa: 1 oa_version: Published Version pmid: 1 publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Developmental emergence of two-stage nonlinear synaptic integration in cerebellar interneurons tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 10 year: '2021' ... --- _id: '9243' abstract: - lang: eng text: Peptidoglycan is an essential component of the bacterial cell envelope that surrounds the cytoplasmic membrane to protect the cell from osmotic lysis. Important antibiotics such as β-lactams and glycopeptides target peptidoglycan biosynthesis. Class A penicillin-binding proteins (PBPs) are bifunctional membrane-bound peptidoglycan synthases that polymerize glycan chains and connect adjacent stem peptides by transpeptidation. How these enzymes work in their physiological membrane environment is poorly understood. Here, we developed a novel Förster resonance energy transfer-based assay to follow in real time both reactions of class A PBPs reconstituted in liposomes or supported lipid bilayers and applied this assay with PBP1B homologues from Escherichia coli, Pseudomonas aeruginosa, and Acinetobacter baumannii in the presence or absence of their cognate lipoprotein activator. Our assay will allow unravelling the mechanisms of peptidoglycan synthesis in a lipid-bilayer environment and can be further developed to be used for high-throughput screening for new antimicrobials. acknowledgement: 'We thank Alexander Egan (Newcastle University) for purified proteins LpoB(sol) and LpoPPa(sol), Federico Corona (Newcastle University) for purified MepM, and Oliver Birkholz and Jacob Piehler (Department of Biology and Center of Cellular Nanoanalytics, University of Osnabru¨ ck) for their help with PBP1B reconstitution into polymer-SLBs and initial guidance on single particle tracking. We also acknowledge Christian P Richter and Changjiang You (Department of Biology and Center of Cellular Nanoanalytics, University of Osnabru¨ ck) for providing SLIMfast software and tris-DODA-NTA reagent, respectively. This work was funded by the BBSRC grant BB/R017409/1 (to WV), the European Research Council through grant ERC-2015-StG-679239 (to ML), and long-term fellowships HFSP LT 000824/2016-L4 and EMBO ALTF 1163–2015 (to NB). ' article_number: 1-32 article_processing_charge: No article_type: original author: - first_name: Víctor M. full_name: Hernández-Rocamora, Víctor M. last_name: Hernández-Rocamora - first_name: Natalia S. full_name: Baranova, Natalia S. id: 38661662-F248-11E8-B48F-1D18A9856A87 last_name: Baranova orcid: 0000-0002-3086-9124 - first_name: Katharina full_name: Peters, Katharina last_name: Peters - first_name: Eefjan full_name: Breukink, Eefjan last_name: Breukink - first_name: Martin full_name: Loose, Martin id: 462D4284-F248-11E8-B48F-1D18A9856A87 last_name: Loose orcid: 0000-0001-7309-9724 - first_name: Waldemar full_name: Vollmer, Waldemar last_name: Vollmer citation: ama: Hernández-Rocamora VM, Baranova NS, Peters K, Breukink E, Loose M, Vollmer W. Real time monitoring of peptidoglycan synthesis by membrane-reconstituted penicillin binding proteins. eLife. 2021;10. doi:10.7554/eLife.61525 apa: Hernández-Rocamora, V. M., Baranova, N. S., Peters, K., Breukink, E., Loose, M., & Vollmer, W. (2021). Real time monitoring of peptidoglycan synthesis by membrane-reconstituted penicillin binding proteins. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.61525 chicago: Hernández-Rocamora, Víctor M., Natalia S. Baranova, Katharina Peters, Eefjan Breukink, Martin Loose, and Waldemar Vollmer. “Real Time Monitoring of Peptidoglycan Synthesis by Membrane-Reconstituted Penicillin Binding Proteins.” ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/eLife.61525. ieee: V. M. Hernández-Rocamora, N. S. Baranova, K. Peters, E. Breukink, M. Loose, and W. Vollmer, “Real time monitoring of peptidoglycan synthesis by membrane-reconstituted penicillin binding proteins,” eLife, vol. 10. eLife Sciences Publications, 2021. ista: Hernández-Rocamora VM, Baranova NS, Peters K, Breukink E, Loose M, Vollmer W. 2021. Real time monitoring of peptidoglycan synthesis by membrane-reconstituted penicillin binding proteins. eLife. 10, 1–32. mla: Hernández-Rocamora, Víctor M., et al. “Real Time Monitoring of Peptidoglycan Synthesis by Membrane-Reconstituted Penicillin Binding Proteins.” ELife, vol. 10, 1–32, eLife Sciences Publications, 2021, doi:10.7554/eLife.61525. short: V.M. Hernández-Rocamora, N.S. Baranova, K. Peters, E. Breukink, M. Loose, W. Vollmer, ELife 10 (2021). date_created: 2021-03-14T23:01:33Z date_published: 2021-02-24T00:00:00Z date_updated: 2024-10-22T10:04:21Z day: '24' ddc: - '570' department: - _id: MaLo doi: 10.7554/eLife.61525 ec_funded: 1 external_id: isi: - '000627596400001' file: - access_level: open_access checksum: 79897a09bfecd9914d39c4aea2841855 content_type: application/pdf creator: dernst date_created: 2021-03-22T07:36:08Z date_updated: 2021-03-22T07:36:08Z file_id: '9268' file_name: 2021_eLife_HernandezRocamora.pdf file_size: 2314698 relation: main_file success: 1 file_date_updated: 2021-03-22T07:36:08Z has_accepted_license: '1' intvolume: ' 10' isi: 1 language: - iso: eng month: '02' oa: 1 oa_version: Published Version project: - _id: 2595697A-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '679239' name: Self-Organization of the Bacterial Cell - _id: 2596EAB6-B435-11E9-9278-68D0E5697425 grant_number: ALTF 2015-1163 name: Synthesis of bacterial cell wall - _id: 259B655A-B435-11E9-9278-68D0E5697425 grant_number: LT000824/2016 name: Reconstitution of bacterial cell wall synthesis publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Real time monitoring of peptidoglycan synthesis by membrane-reconstituted penicillin binding proteins tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 10 year: '2021' ... --- _id: '9746' abstract: - lang: eng text: Evolutionary adaptation is a major source of antibiotic resistance in bacterial pathogens. Evolution-informed therapy aims to constrain resistance by accounting for bacterial evolvability. Sequential treatments with antibiotics that target different bacterial processes were previously shown to limit adaptation through genetic resistance trade-offs and negative hysteresis. Treatment with homogeneous sets of antibiotics is generally viewed to be disadvantageous, as it should rapidly lead to cross-resistance. We here challenged this assumption by determining the evolutionary response of Pseudomonas aeruginosa to experimental sequential treatments involving both heterogenous and homogeneous antibiotic sets. To our surprise, we found that fast switching between only β-lactam antibiotics resulted in increased extinction of bacterial populations. We demonstrate that extinction is favored by low rates of spontaneous resistance emergence and low levels of spontaneous cross-resistance among the antibiotics in sequence. The uncovered principles may help to guide the optimized use of available antibiotics in highly potent, evolution-informed treatment designs. acknowledgement: We would like to thank Leif Tueffers and João Botelho for discussions and suggestions as well as Kira Haas and Julia Bunk for technical support. We acknowledge financial support from the German Science Foundation (grant SCHU 1415/12-2 to HS, and funding under Germany’s Excellence Strategy EXC 2167–390884018 as well as the Research Training Group 2501 TransEvo to HS and SN), the Max Planck Society (IMPRS scholarship to AB; Max-Planck fellowship to HS), and the Leibniz Science Campus Evolutionary Medicine of the Lung (EvoLUNG, to HS and SN). This work was further supported by the German Science Foundation Research Infrastructure NGS_CC (project 407495230) as part of the Next Generation Sequencing Competence Network (project 423957469). NGS analyses were carried out at the Competence Centre for Genomic Analysis Kiel (CCGA Kiel). article_number: e68876 article_processing_charge: No article_type: original author: - first_name: Aditi full_name: Batra, Aditi last_name: Batra - first_name: Roderich full_name: Römhild, Roderich id: 68E56E44-62B0-11EA-B963-444F3DDC885E last_name: Römhild orcid: 0000-0001-9480-5261 - first_name: Emilie full_name: Rousseau, Emilie last_name: Rousseau - first_name: Sören full_name: Franzenburg, Sören last_name: Franzenburg - first_name: Stefan full_name: Niemann, Stefan last_name: Niemann - first_name: Hinrich full_name: Schulenburg, Hinrich last_name: Schulenburg citation: ama: Batra A, Römhild R, Rousseau E, Franzenburg S, Niemann S, Schulenburg H. High potency of sequential therapy with only beta-lactam antibiotics. eLife. 2021;10. doi:10.7554/elife.68876 apa: Batra, A., Römhild, R., Rousseau, E., Franzenburg, S., Niemann, S., & Schulenburg, H. (2021). High potency of sequential therapy with only beta-lactam antibiotics. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.68876 chicago: Batra, Aditi, Roderich Römhild, Emilie Rousseau, Sören Franzenburg, Stefan Niemann, and Hinrich Schulenburg. “High Potency of Sequential Therapy with Only Beta-Lactam Antibiotics.” ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/elife.68876. ieee: A. Batra, R. Römhild, E. Rousseau, S. Franzenburg, S. Niemann, and H. Schulenburg, “High potency of sequential therapy with only beta-lactam antibiotics,” eLife, vol. 10. eLife Sciences Publications, 2021. ista: Batra A, Römhild R, Rousseau E, Franzenburg S, Niemann S, Schulenburg H. 2021. High potency of sequential therapy with only beta-lactam antibiotics. eLife. 10, e68876. mla: Batra, Aditi, et al. “High Potency of Sequential Therapy with Only Beta-Lactam Antibiotics.” ELife, vol. 10, e68876, eLife Sciences Publications, 2021, doi:10.7554/elife.68876. short: A. Batra, R. Römhild, E. Rousseau, S. Franzenburg, S. Niemann, H. Schulenburg, ELife 10 (2021). date_created: 2021-07-28T13:36:57Z date_published: 2021-07-28T00:00:00Z date_updated: 2023-08-11T10:26:29Z day: '28' department: - _id: CaGu doi: 10.7554/elife.68876 external_id: isi: - '000692027800001' pmid: - '34318749' intvolume: ' 10' isi: 1 language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.7554/eLife.68876 month: '07' oa: 1 oa_version: Published Version pmid: 1 publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: High potency of sequential therapy with only beta-lactam antibiotics type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 10 year: '2021' ... --- _id: '9999' abstract: - lang: eng text: 'The developmental strategies used by progenitor cells to endure a safe journey from their induction place towards the site of terminal differentiation are still poorly understood. Here we uncovered a progenitor cell allocation mechanism that stems from an incomplete process of epithelial delamination that allows progenitors to coordinate their movement with adjacent extra-embryonic tissues. Progenitors of the zebrafish laterality organ originate from the surface epithelial enveloping layer by an apical constriction process of cell delamination. During this process, progenitors retain long-term apical contacts that enable the epithelial layer to pull a subset of progenitors along their way towards the vegetal pole. The remaining delaminated progenitors follow apically-attached progenitors’ movement by a co-attraction mechanism, avoiding sequestration by the adjacent endoderm, ensuring their fate and collective allocation at the differentiation site. Thus, we reveal that incomplete delamination serves as a cellular platform for coordinated tissue movements during development. Impact Statement: Incomplete delamination serves as a cellular platform for coordinated tissue movements during development, guiding newly formed progenitor cell groups to the differentiation site.' article_number: e66483 article_processing_charge: Yes article_type: original author: - first_name: Eduardo full_name: Pulgar, Eduardo last_name: Pulgar - first_name: Cornelia full_name: Schwayer, Cornelia id: 3436488C-F248-11E8-B48F-1D18A9856A87 last_name: Schwayer orcid: 0000-0001-5130-2226 - first_name: Néstor full_name: Guerrero, Néstor last_name: Guerrero - first_name: Loreto full_name: López, Loreto last_name: López - first_name: Susana full_name: Márquez, Susana last_name: Márquez - first_name: Steffen full_name: Härtel, Steffen last_name: Härtel - first_name: Rodrigo full_name: Soto, Rodrigo last_name: Soto - first_name: Carl Philipp full_name: Heisenberg, Carl Philipp last_name: Heisenberg - first_name: Miguel L. full_name: Concha, Miguel L. last_name: Concha citation: ama: Pulgar E, Schwayer C, Guerrero N, et al. Apical contacts stemming from incomplete delamination guide progenitor cell allocation through a dragging mechanism. eLife. 2021;10. doi:10.7554/eLife.66483 apa: Pulgar, E., Schwayer, C., Guerrero, N., López, L., Márquez, S., Härtel, S., … Concha, M. L. (2021). Apical contacts stemming from incomplete delamination guide progenitor cell allocation through a dragging mechanism. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.66483 chicago: Pulgar, Eduardo, Cornelia Schwayer, Néstor Guerrero, Loreto López, Susana Márquez, Steffen Härtel, Rodrigo Soto, Carl Philipp Heisenberg, and Miguel L. Concha. “Apical Contacts Stemming from Incomplete Delamination Guide Progenitor Cell Allocation through a Dragging Mechanism.” ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/eLife.66483. ieee: E. Pulgar et al., “Apical contacts stemming from incomplete delamination guide progenitor cell allocation through a dragging mechanism,” eLife, vol. 10. eLife Sciences Publications, 2021. ista: Pulgar E, Schwayer C, Guerrero N, López L, Márquez S, Härtel S, Soto R, Heisenberg CP, Concha ML. 2021. Apical contacts stemming from incomplete delamination guide progenitor cell allocation through a dragging mechanism. eLife. 10, e66483. mla: Pulgar, Eduardo, et al. “Apical Contacts Stemming from Incomplete Delamination Guide Progenitor Cell Allocation through a Dragging Mechanism.” ELife, vol. 10, e66483, eLife Sciences Publications, 2021, doi:10.7554/eLife.66483. short: E. Pulgar, C. Schwayer, N. Guerrero, L. López, S. Márquez, S. Härtel, R. Soto, C.P. Heisenberg, M.L. Concha, ELife 10 (2021). date_created: 2021-09-12T22:01:23Z date_published: 2021-08-27T00:00:00Z date_updated: 2025-04-14T07:46:58Z day: '27' ddc: - '570' department: - _id: CaHe doi: 10.7554/eLife.66483 ec_funded: 1 external_id: isi: - '000700428500001' pmid: - '34448451' file: - access_level: open_access checksum: a3f82b0499cc822ac1eab48a01f3f57e content_type: application/pdf creator: dernst date_created: 2022-05-13T08:03:37Z date_updated: 2022-05-13T08:03:37Z file_id: '11371' file_name: 2021_eLife_Pulgar.pdf file_size: 9010446 relation: main_file success: 1 file_date_updated: 2022-05-13T08:03:37Z has_accepted_license: '1' intvolume: ' 10' isi: 1 keyword: - cell delamination - apical constriction - dragging - mechanical forces - collective 18 locomotion - dorsal forerunner cells - zebrafish language: - iso: eng month: '08' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 260F1432-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '742573' name: Interaction and feedback between cell mechanics and fate specification in vertebrate gastrulation publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Apical contacts stemming from incomplete delamination guide progenitor cell allocation through a dragging mechanism tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 10 year: '2021' ...