[{"quality_controlled":"1","citation":{"ieee":"I. Kulich, J. Schmid, A. Teplova, L. Qi, and J. Friml, “Rapid translocation of NGR proteins driving polarization of PIN-activating D6 protein kinase during root gravitropism,” <i>eLife</i>, vol. 12. eLife Sciences Publications, 2024.","mla":"Kulich, Ivan, et al. “Rapid Translocation of NGR Proteins Driving Polarization of PIN-Activating D6 Protein Kinase during Root Gravitropism.” <i>ELife</i>, vol. 12, 91523, eLife Sciences Publications, 2024, doi:<a href=\"https://doi.org/10.7554/elife.91523\">10.7554/elife.91523</a>.","apa":"Kulich, I., Schmid, J., Teplova, A., Qi, L., &#38; Friml, J. (2024). Rapid translocation of NGR proteins driving polarization of PIN-activating D6 protein kinase during root gravitropism. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.91523\">https://doi.org/10.7554/elife.91523</a>","ista":"Kulich I, Schmid J, Teplova A, Qi L, Friml J. 2024. Rapid translocation of NGR proteins driving polarization of PIN-activating D6 protein kinase during root gravitropism. eLife. 12, 91523.","chicago":"Kulich, Ivan, Julia Schmid, Anastasiia Teplova, Linlin Qi, and Jiří Friml. “Rapid Translocation of NGR Proteins Driving Polarization of PIN-Activating D6 Protein Kinase during Root Gravitropism.” <i>ELife</i>. eLife Sciences Publications, 2024. <a href=\"https://doi.org/10.7554/elife.91523\">https://doi.org/10.7554/elife.91523</a>.","ama":"Kulich I, Schmid J, Teplova A, Qi L, Friml J. Rapid translocation of NGR proteins driving polarization of PIN-activating D6 protein kinase during root gravitropism. <i>eLife</i>. 2024;12. doi:<a href=\"https://doi.org/10.7554/elife.91523\">10.7554/elife.91523</a>","short":"I. Kulich, J. Schmid, A. Teplova, L. Qi, J. Friml, ELife 12 (2024)."},"file_date_updated":"2024-04-03T13:18:00Z","article_number":"91523","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"issn":["2050-084X"]},"acknowledged_ssus":[{"_id":"LifeSc"},{"_id":"Bio"}],"doi":"10.7554/elife.91523","has_accepted_license":"1","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"corr_author":"1","oa":1,"external_id":{"pmid":["38441122"]},"related_material":{"link":[{"relation":"press_release","url":"https://ista.ac.at/en/news/beneath-the-surface/","description":"News on ISTA website"}]},"date_updated":"2025-04-23T07:45:02Z","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"volume":12,"DOAJ_listed":"1","department":[{"_id":"JiFr"}],"publication":"eLife","_id":"15257","abstract":[{"text":"Root gravitropic bending represents a fundamental aspect of terrestrial plant physiology. Gravity is perceived by sedimentation of starch-rich plastids (statoliths) to the bottom of the central root cap cells. Following gravity perception, intercellular auxin transport is redirected downwards leading to an asymmetric auxin accumulation at the lower root side causing inhibition of cell expansion, ultimately resulting in downwards bending. How gravity-induced statoliths repositioning is translated into asymmetric auxin distribution remains unclear despite PIN auxin efflux carriers and the Negative Gravitropic Response of roots (NGR) proteins polarize along statolith sedimentation, thus providing a plausible mechanism for auxin flow redirection. In this study, using a functional NGR1-GFP construct, we visualized the NGR1 localization on the statolith surface and plasma membrane (PM) domains in close proximity to the statoliths, correlating with their movements. We determined that NGR1 binding to these PM domains is indispensable for NGR1 functionality and relies on cysteine acylation and adjacent polybasic regions as well as on lipid and sterol PM composition. Detailed timing of the early events following graviperception suggested that both NGR1 repolarization and initial auxin asymmetry precede the visible PIN3 polarization. This discrepancy motivated us to unveil a rapid, NGR-dependent translocation of PIN-activating AGCVIII kinase D6PK towards lower PMs of gravity-perceiving cells, thus providing an attractive model for rapid redirection of auxin fluxes following gravistimulation.","lang":"eng"}],"intvolume":"        12","file":[{"creator":"dernst","checksum":"a73a84d3bf97a6d09d24308ca6dd0a0c","file_id":"15288","date_created":"2024-04-03T13:18:00Z","success":1,"file_size":11451904,"content_type":"application/pdf","relation":"main_file","date_updated":"2024-04-03T13:18:00Z","access_level":"open_access","file_name":"2024_eLife_Kulich.pdf"}],"article_type":"original","month":"03","pmid":1,"oa_version":"Published Version","ec_funded":1,"title":"Rapid translocation of NGR proteins driving polarization of PIN-activating D6 protein kinase during root gravitropism","article_processing_charge":"Yes","year":"2024","author":[{"full_name":"Kulich, Ivan","first_name":"Ivan","id":"57a1567c-8314-11eb-9063-c9ddc3451a54","last_name":"Kulich"},{"last_name":"Schmid","id":"07cf4637-baaf-11ee-9227-e1de57d1d69b","full_name":"Schmid, Julia","first_name":"Julia"},{"first_name":"Anastasiia","full_name":"Teplova, Anastasiia","id":"e3736151-106c-11ec-b916-c2558e2762c6","last_name":"Teplova"},{"id":"44B04502-A9ED-11E9-B6FC-583AE6697425","last_name":"Qi","first_name":"Linlin","full_name":"Qi, Linlin","orcid":"0000-0001-5187-8401"},{"last_name":"Friml","id":"4159519E-F248-11E8-B48F-1D18A9856A87","full_name":"Friml, Jiří","first_name":"Jiří","orcid":"0000-0002-8302-7596"}],"status":"public","date_created":"2024-04-02T11:35:58Z","acknowledgement":"The research leading to these results has received funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme grant agreement No 742985 and Austrian Science Fund (FWF): I3630-775 B25 to J.F. This research was also supported by the Lab Support Facility (LSF) and the Imaging and Optics Facility (IOF) of IST Austria, namely Tereza Bělinová for her help with the imaging. JS was supported by FemTECH fellowship.","project":[{"grant_number":"742985","name":"Tracing Evolution of Auxin Transport and Polarity in Plants","call_identifier":"H2020","_id":"261099A6-B435-11E9-9278-68D0E5697425"},{"call_identifier":"FWF","_id":"26538374-B435-11E9-9278-68D0E5697425","name":"Molecular mechanisms of endocytic cargo recognition in plants","grant_number":"I03630"}],"publication_status":"published","publisher":"eLife Sciences Publications","date_published":"2024-03-05T00:00:00Z","language":[{"iso":"eng"}],"scopus_import":"1","type":"journal_article","day":"05","ddc":["580"],"license":"https://creativecommons.org/licenses/by/4.0/"},{"publisher":"Elsevier","publication_status":"published","project":[{"name":"Role of Eed in neural stem cell lineage progression","grant_number":"T01031","call_identifier":"FWF","_id":"268F8446-B435-11E9-9278-68D0E5697425"},{"_id":"260C2330-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","name":"ISTplus - Postdoctoral Fellowships","grant_number":"754411"},{"_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E","name":"Stem Cell Modulation in Neural Development and Regeneration/ P05-Molecular Mechanisms of Neural Stem Cell Lineage Progression","grant_number":"F7805"},{"_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"}],"acknowledgement":"This research was supported by the Scientific Service Units (SSU) at IST Austria through resources provided by the Imaging & Optics Facility (IOF) and Preclinical Facilities (PCF). N.A. received support from FWF Firnberg-Programme (T 1031). G.C. received support from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 754411 as an ISTplus postdoctoral fellow. This work was also supported by IST Austria institutional funds, FWF SFB F78 to S.H., and the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 725780 LinPro) to S.H.","date_created":"2023-12-13T11:48:05Z","status":"public","author":[{"last_name":"Amberg","id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","full_name":"Amberg, Nicole","first_name":"Nicole","orcid":"0000-0002-3183-8207"},{"full_name":"Cheung, Giselle T","first_name":"Giselle T","id":"471195F6-F248-11E8-B48F-1D18A9856A87","last_name":"Cheung","orcid":"0000-0001-8457-2572"},{"first_name":"Simon","full_name":"Hippenmeyer, Simon","last_name":"Hippenmeyer","id":"37B36620-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2279-1061"}],"year":"2024","title":"Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry","article_processing_charge":"Yes (in subscription journal)","ec_funded":1,"oa_version":"Published Version","pmid":1,"ddc":["570"],"day":"15","type":"journal_article","scopus_import":"1","language":[{"iso":"eng"}],"date_published":"2024-03-15T00:00:00Z","issue":"1","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"has_accepted_license":"1","doi":"10.1016/j.xpro.2023.102771","acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"publication_identifier":{"issn":["2666-1667"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_number":"102771","citation":{"ieee":"N. Amberg, G. T. Cheung, and S. Hippenmeyer, “Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry,” <i>STAR Protocols</i>, vol. 5, no. 1. Elsevier, 2024.","chicago":"Amberg, Nicole, Giselle T Cheung, and Simon Hippenmeyer. “Protocol for Sorting Cells from Mouse Brains Labeled with Mosaic Analysis with Double Markers by Flow Cytometry.” <i>STAR Protocols</i>. Elsevier, 2024. <a href=\"https://doi.org/10.1016/j.xpro.2023.102771\">https://doi.org/10.1016/j.xpro.2023.102771</a>.","mla":"Amberg, Nicole, et al. “Protocol for Sorting Cells from Mouse Brains Labeled with Mosaic Analysis with Double Markers by Flow Cytometry.” <i>STAR Protocols</i>, vol. 5, no. 1, 102771, Elsevier, 2024, doi:<a href=\"https://doi.org/10.1016/j.xpro.2023.102771\">10.1016/j.xpro.2023.102771</a>.","ista":"Amberg N, Cheung GT, Hippenmeyer S. 2024. Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols. 5(1), 102771.","apa":"Amberg, N., Cheung, G. T., &#38; Hippenmeyer, S. (2024). Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. <i>STAR Protocols</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.xpro.2023.102771\">https://doi.org/10.1016/j.xpro.2023.102771</a>","ama":"Amberg N, Cheung GT, Hippenmeyer S. Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. <i>STAR Protocols</i>. 2024;5(1). doi:<a href=\"https://doi.org/10.1016/j.xpro.2023.102771\">10.1016/j.xpro.2023.102771</a>","short":"N. Amberg, G.T. Cheung, S. Hippenmeyer, STAR Protocols 5 (2024)."},"file_date_updated":"2024-07-16T11:50:03Z","quality_controlled":"1","article_type":"review","month":"03","file":[{"file_name":"2024_STARProtoc_Amberg.pdf","relation":"main_file","date_updated":"2024-07-16T11:50:03Z","access_level":"open_access","file_id":"17260","content_type":"application/pdf","file_size":8871807,"success":1,"date_created":"2024-07-16T11:50:03Z","creator":"dernst","checksum":"3f0ee62e04bf5a44b45b035662826e95"}],"abstract":[{"lang":"eng","text":"Mosaic analysis with double markers (MADM) technology enables the generation of genetic mosaic tissue in mice and high-resolution phenotyping at the individual cell level. Here, we present a protocol for isolating MADM-labeled cells with high yield for downstream molecular analyses using fluorescence-activated cell sorting (FACS). We describe steps for generating MADM-labeled mice, perfusion, single-cell suspension, and debris removal. We then detail procedures for cell sorting by FACS and downstream analysis. This protocol is suitable for embryonic to adult mice.\r\nFor complete details on the use and execution of this protocol, please refer to Contreras et al. (2021).1"}],"_id":"14683","intvolume":"         5","publication":"STAR Protocols","department":[{"_id":"SiHi"}],"volume":5,"keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Neuroscience"],"date_updated":"2025-04-15T08:23:06Z","external_id":{"pmid":["38070137"]},"oa":1,"corr_author":"1"},{"scopus_import":"1","isi":1,"language":[{"iso":"eng"}],"ddc":["580"],"day":"21","type":"journal_article","APC_amount":"2792,52 EUR","date_published":"2024-02-21T00:00:00Z","project":[{"name":"Tracing Evolution of Auxin Transport and Polarity in Plants","grant_number":"742985","call_identifier":"H2020","_id":"261099A6-B435-11E9-9278-68D0E5697425"},{"grant_number":"I03630","name":"Molecular mechanisms of endocytic cargo recognition in plants","_id":"26538374-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"name":"FWF Open Access Fund","call_identifier":"FWF","_id":"3AC91DDA-15DF-11EA-824D-93A3E7B544D1"}],"acknowledgement":"The authors would like to gratefully acknowledge Dr Xixi Zhang for cloning the GNL1/pDONR221 construct and for useful discussions.H2020 European Research Council Advanced Grant ETAP742985 to Jiří Friml, Austrian Science Fund I 3630-B25 to Jiří Friml","date_created":"2024-02-27T07:10:11Z","status":"public","publisher":"eLife Sciences Publications","publication_status":"published","article_processing_charge":"Yes","title":"Developmental patterning function of GNOM ARF-GEF mediated from the cell periphery","oa_version":"Published Version","ec_funded":1,"pmid":1,"OA_place":"publisher","author":[{"orcid":"0000-0001-6463-5257","full_name":"Adamowski, Maciek","first_name":"Maciek","id":"45F536D2-F248-11E8-B48F-1D18A9856A87","last_name":"Adamowski"},{"last_name":"Matijevic","id":"83c17ce3-15b2-11ec-abd3-f486545870bd","first_name":"Ivana","full_name":"Matijevic, Ivana"},{"orcid":"0000-0002-8302-7596","full_name":"Friml, Jiří","first_name":"Jiří","id":"4159519E-F248-11E8-B48F-1D18A9856A87","last_name":"Friml"}],"year":"2024","publication":"eLife","department":[{"_id":"JiFr"}],"DOAJ_listed":"1","volume":13,"keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"article_type":"original","month":"02","file":[{"creator":"dernst","checksum":"b2b2d583b433823af731842f1420113e","file_id":"17310","success":1,"file_size":15675744,"date_created":"2024-07-22T11:51:50Z","content_type":"application/pdf","relation":"main_file","date_updated":"2024-07-22T11:51:50Z","access_level":"open_access","file_name":"2024_eLife_Adamowski.pdf"}],"intvolume":"        13","_id":"15033","abstract":[{"lang":"eng","text":"The GNOM (GN) Guanine nucleotide Exchange Factor for ARF small GTPases (ARF-GEF) is among the best studied trafficking regulators in plants, playing crucial and unique developmental roles in patterning and polarity. The current models place GN at the Golgi apparatus (GA), where it mediates secretion/recycling, and at the plasma membrane (PM) presumably contributing to clathrin-mediated endocytosis (CME). The mechanistic basis of the developmental function of GN, distinct from the other ARF-GEFs including its closest homologue GNOM-LIKE1 (GNL1), remains elusive. Insights from this study largely extend the current notions of GN function. We show that GN, but not GNL1, localizes to the cell periphery at long-lived structures distinct from clathrin-coated pits, while CME and secretion proceed normally in <jats:italic>gn</jats:italic> knockouts. The functional GN mutant variant GN<jats:sup>fewerroots</jats:sup>, absent from the GA, suggests that the cell periphery is the major site of GN action responsible for its developmental function. Following inhibition by Brefeldin A, GN, but not GNL1, relocates to the PM likely on exocytic vesicles, suggesting selective molecular associations en route to the cell periphery. A study of GN-GNL1 chimeric ARF-GEFs indicates that all GN domains contribute to the specific GN function in a partially redundant manner. Together, this study offers significant steps toward the elucidation of the mechanism underlying unique cellular and development functions of GNOM."}],"oa":1,"corr_author":"1","date_updated":"2025-10-15T06:31:47Z","external_id":{"isi":["001174278000001"],"pmid":["38381485"]},"publication_identifier":{"issn":["2050-084X"]},"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"has_accepted_license":"1","doi":"10.7554/elife.68993","quality_controlled":"1","OA_type":"gold","user_id":"317138e5-6ab7-11ef-aa6d-ffef3953e345","file_date_updated":"2024-07-22T11:51:50Z","citation":{"chicago":"Adamowski, Maciek, Ivana Matijevic, and Jiří Friml. “Developmental Patterning Function of GNOM ARF-GEF Mediated from the Cell Periphery.” <i>ELife</i>. eLife Sciences Publications, 2024. <a href=\"https://doi.org/10.7554/elife.68993\">https://doi.org/10.7554/elife.68993</a>.","ista":"Adamowski M, Matijevic I, Friml J. 2024. Developmental patterning function of GNOM ARF-GEF mediated from the cell periphery. eLife. 13.","mla":"Adamowski, Maciek, et al. “Developmental Patterning Function of GNOM ARF-GEF Mediated from the Cell Periphery.” <i>ELife</i>, vol. 13, eLife Sciences Publications, 2024, doi:<a href=\"https://doi.org/10.7554/elife.68993\">10.7554/elife.68993</a>.","apa":"Adamowski, M., Matijevic, I., &#38; Friml, J. (2024). Developmental patterning function of GNOM ARF-GEF mediated from the cell periphery. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.68993\">https://doi.org/10.7554/elife.68993</a>","ieee":"M. Adamowski, I. Matijevic, and J. Friml, “Developmental patterning function of GNOM ARF-GEF mediated from the cell periphery,” <i>eLife</i>, vol. 13. eLife Sciences Publications, 2024.","short":"M. Adamowski, I. Matijevic, J. Friml, ELife 13 (2024).","ama":"Adamowski M, Matijevic I, Friml J. Developmental patterning function of GNOM ARF-GEF mediated from the cell periphery. <i>eLife</i>. 2024;13. doi:<a href=\"https://doi.org/10.7554/elife.68993\">10.7554/elife.68993</a>"}},{"has_accepted_license":"1","doi":"10.1016/j.xpro.2022.101866","tmp":{"image":"/images/cc_by_nc_nd.png","name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)"},"publication_identifier":{"issn":["2666-1667"]},"acknowledged_ssus":[{"_id":"Bio"}],"article_number":"101866","file_date_updated":"2023-01-23T09:50:51Z","citation":{"ieee":"V. Hübschmann, M. Korkut, and S. Siegert, “Assessing human iPSC-derived microglia identity and function by immunostaining, phagocytosis, calcium activity, and inflammation assay,” <i>STAR Protocols</i>, vol. 3, no. 4. Elsevier, 2022.","chicago":"Hübschmann, Verena, Medina Korkut, and Sandra Siegert. “Assessing Human IPSC-Derived Microglia Identity and Function by Immunostaining, Phagocytosis, Calcium Activity, and Inflammation Assay.” <i>STAR Protocols</i>. Elsevier, 2022. <a href=\"https://doi.org/10.1016/j.xpro.2022.101866\">https://doi.org/10.1016/j.xpro.2022.101866</a>.","ista":"Hübschmann V, Korkut M, Siegert S. 2022. Assessing human iPSC-derived microglia identity and function by immunostaining, phagocytosis, calcium activity, and inflammation assay. STAR Protocols. 3(4), 101866.","apa":"Hübschmann, V., Korkut, M., &#38; Siegert, S. (2022). Assessing human iPSC-derived microglia identity and function by immunostaining, phagocytosis, calcium activity, and inflammation assay. <i>STAR Protocols</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.xpro.2022.101866\">https://doi.org/10.1016/j.xpro.2022.101866</a>","mla":"Hübschmann, Verena, et al. “Assessing Human IPSC-Derived Microglia Identity and Function by Immunostaining, Phagocytosis, Calcium Activity, and Inflammation Assay.” <i>STAR Protocols</i>, vol. 3, no. 4, 101866, Elsevier, 2022, doi:<a href=\"https://doi.org/10.1016/j.xpro.2022.101866\">10.1016/j.xpro.2022.101866</a>.","ama":"Hübschmann V, Korkut M, Siegert S. Assessing human iPSC-derived microglia identity and function by immunostaining, phagocytosis, calcium activity, and inflammation assay. <i>STAR Protocols</i>. 2022;3(4). doi:<a href=\"https://doi.org/10.1016/j.xpro.2022.101866\">10.1016/j.xpro.2022.101866</a>","short":"V. Hübschmann, M. Korkut, S. Siegert, STAR Protocols 3 (2022)."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","quality_controlled":"1","file":[{"access_level":"open_access","date_updated":"2023-01-23T09:50:51Z","relation":"main_file","file_name":"2022_STARProtocols_Huebschmann.pdf","checksum":"3c71b8a60633d42c2f77c49025d5559b","creator":"dernst","date_created":"2023-01-23T09:50:51Z","success":1,"file_size":6251945,"content_type":"application/pdf","file_id":"12340"}],"_id":"12117","abstract":[{"text":"To understand how potential gene manipulations affect in vitro microglia, we provide a set of short protocols to evaluate microglia identity and function. We detail steps for immunostaining to determine microglia identity. We describe three functional assays for microglia: phagocytosis, calcium response following ATP stimulation, and cytokine expression upon inflammatory stimuli. We apply these protocols to human induced-pluripotent-stem-cell (hiPSC)-derived microglia, but they can be also applied to other in vitro microglial models including primary mouse microglia.\r\nFor complete details on the use and execution of this protocol, please refer to Bartalska et al. (2022).1","lang":"eng"}],"intvolume":"         3","month":"12","article_type":"letter_note","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Neuroscience"],"volume":3,"publication":"STAR Protocols","department":[{"_id":"SaSi"},{"_id":"GradSch"}],"date_updated":"2025-06-11T13:58:47Z","related_material":{"record":[{"id":"11478","relation":"other","status":"public"}]},"external_id":{"pmid":["36595902"]},"oa":1,"corr_author":"1","publication_status":"published","publisher":"Elsevier","acknowledgement":"This project has received funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program (grant No. 715571 to S.S.) and from the Gesellschaft für Forschungsförderung Niederösterreich (grant No. Sc19-017 to V.H.). We thank Rouven Schulz and Alessandro Venturino for their insights into functional assays and data analysis, Verena Seiboth for insights into necessary institutional permission, and ISTA imaging & optics facility (IOF) especially Bernhard Hochreiter for their support.","date_created":"2023-01-12T11:56:38Z","status":"public","project":[{"grant_number":"715571","name":"Microglia action towards neuronal circuit formation and function in health and disease","_id":"25D4A630-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"grant_number":"SC19-017","name":"How human microglia shape developing neurons during health and inflammation","_id":"9B99D380-BA93-11EA-9121-9846C619BF3A"}],"author":[{"first_name":"Verena","full_name":"Hübschmann, Verena","last_name":"Hübschmann","id":"32B7C918-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Korkut","id":"4B51CE74-F248-11E8-B48F-1D18A9856A87","first_name":"Medina","full_name":"Korkut, Medina","orcid":"0000-0003-4309-2251"},{"orcid":"0000-0001-8635-0877","last_name":"Siegert","id":"36ACD32E-F248-11E8-B48F-1D18A9856A87","full_name":"Siegert, Sandra","first_name":"Sandra"}],"year":"2022","pmid":1,"title":"Assessing human iPSC-derived microglia identity and function by immunostaining, phagocytosis, calcium activity, and inflammation assay","article_processing_charge":"No","oa_version":"Published Version","ec_funded":1,"day":"16","ddc":["570"],"type":"journal_article","license":"https://creativecommons.org/licenses/by-nc-nd/4.0/","language":[{"iso":"eng"}],"scopus_import":"1","date_published":"2022-12-16T00:00:00Z","issue":"4"},{"author":[{"last_name":"Hayward","id":"fc885ee5-24bf-11eb-ad7b-bcc5104c0c1b","full_name":"Hayward, Laura","first_name":"Laura"},{"full_name":"Sella, Guy","first_name":"Guy","last_name":"Sella"}],"year":"2022","article_processing_charge":"No","title":"Polygenic adaptation after a sudden change in environment","oa_version":"Published Version","publisher":"eLife Sciences Publications","publication_status":"published","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","status":"public","date_created":"2023-01-12T12:09:00Z","date_published":"2022-09-26T00:00:00Z","day":"26","ddc":["570"],"type":"journal_article","scopus_import":"1","isi":1,"language":[{"iso":"eng"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","article_number":"66697","file_date_updated":"2023-01-24T12:21:32Z","citation":{"ama":"Hayward L, Sella G. Polygenic adaptation after a sudden change in environment. <i>eLife</i>. 2022;11. doi:<a href=\"https://doi.org/10.7554/elife.66697\">10.7554/elife.66697</a>","short":"L. Hayward, G. Sella, ELife 11 (2022).","ieee":"L. Hayward and G. Sella, “Polygenic adaptation after a sudden change in environment,” <i>eLife</i>, 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.” <i>ELife</i>, vol. 11, 66697, eLife Sciences Publications, 2022, doi:<a href=\"https://doi.org/10.7554/elife.66697\">10.7554/elife.66697</a>.","apa":"Hayward, L., &#38; Sella, G. (2022). Polygenic adaptation after a sudden change in environment. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.66697\">https://doi.org/10.7554/elife.66697</a>","chicago":"Hayward, Laura, and Guy Sella. “Polygenic Adaptation after a Sudden Change in Environment.” <i>ELife</i>. eLife Sciences Publications, 2022. <a href=\"https://doi.org/10.7554/elife.66697\">https://doi.org/10.7554/elife.66697</a>."},"quality_controlled":"1","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"has_accepted_license":"1","doi":"10.7554/elife.66697","publication_identifier":{"eissn":["2050-084X"]},"date_updated":"2024-10-09T21:03:38Z","external_id":{"isi":["000890735600001"]},"oa":1,"corr_author":"1","article_type":"original","month":"09","file":[{"creator":"dernst","checksum":"28de155b231ac1c8d4501c98b2fb359a","file_id":"12363","success":1,"date_created":"2023-01-24T12:21:32Z","file_size":18935612,"content_type":"application/pdf","relation":"main_file","date_updated":"2023-01-24T12:21:32Z","access_level":"open_access","file_name":"2022_eLife_Hayward.pdf"}],"_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."}],"intvolume":"        11","publication":"eLife","department":[{"_id":"NiBa"}],"volume":11,"keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"]},{"author":[{"orcid":"0000-0001-8619-2223","first_name":"Andreas","full_name":"Angermayr, Andreas","id":"4677C796-F248-11E8-B48F-1D18A9856A87","last_name":"Angermayr"},{"last_name":"Pang","full_name":"Pang, Tin Yau","first_name":"Tin Yau"},{"first_name":"Guillaume","full_name":"Chevereau, Guillaume","last_name":"Chevereau"},{"last_name":"Mitosch","id":"39B66846-F248-11E8-B48F-1D18A9856A87","first_name":"Karin","full_name":"Mitosch, Karin"},{"last_name":"Lercher","full_name":"Lercher, Martin J","first_name":"Martin J"},{"last_name":"Bollenbach","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","full_name":"Bollenbach, Mark Tobias","first_name":"Mark Tobias","orcid":"0000-0003-4398-476X"}],"year":"2022","article_processing_charge":"No","title":"Growth‐mediated negative feedback shapes quantitative antibiotic response","oa_version":"Published Version","pmid":1,"publisher":"Embo Press","publication_status":"published","acknowledgement":"This work was in part supported by Human Frontier Science Program GrantRGP0042/2013, Marie Curie Career Integration Grant303507, AustrianScience Fund (FWF) Grant P27201-B22, and German Research Foundation(DFG) Collaborative Research Center (SFB)1310to TB. SAA was supportedby the European Union’s Horizon2020Research and Innovation Programunder the Marie Skłodowska-Curie Grant agreement No707352. We wouldlike to thank the Bollenbach group for regular fruitful discussions. We areparticularly thankful for the technical assistance of Booshini Fernando andfor discussions of the theoretical aspects with Gerrit Ansmann. We areindebted to Bor Kavˇciˇc for invaluable advice, help with setting up theluciferase-based growth monitoring system, and for sharing plasmids. Weacknowledge the IST Austria Miba Machine Shop for their support inbuilding a housing for the stacker of the plate reader, which enabled thehigh-throughput luciferase-based experiments. We are grateful to RosalindAllen, Bor Kavˇciˇc and Dor Russ for feedback on the manuscript. Open Accessfunding enabled and organized by Projekt DEAL.","status":"public","date_created":"2023-01-16T09:58:34Z","date_published":"2022-09-01T00:00:00Z","issue":"9","day":"01","ddc":["570"],"type":"journal_article","scopus_import":"1","isi":1,"language":[{"iso":"eng"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_number":"e10490","file_date_updated":"2023-01-30T09:49:55Z","citation":{"ieee":"A. Angermayr, T. Y. Pang, G. Chevereau, K. Mitosch, M. J. Lercher, and M. T. Bollenbach, “Growth‐mediated negative feedback shapes quantitative antibiotic response,” <i>Molecular Systems Biology</i>, vol. 18, no. 9. Embo Press, 2022.","chicago":"Angermayr, Andreas, Tin Yau Pang, Guillaume Chevereau, Karin Mitosch, Martin J Lercher, and Mark Tobias Bollenbach. “Growth‐mediated Negative Feedback Shapes Quantitative Antibiotic Response.” <i>Molecular Systems Biology</i>. Embo Press, 2022. <a href=\"https://doi.org/10.15252/msb.202110490\">https://doi.org/10.15252/msb.202110490</a>.","ista":"Angermayr A, Pang TY, Chevereau G, Mitosch K, Lercher MJ, Bollenbach MT. 2022. Growth‐mediated negative feedback shapes quantitative antibiotic response. Molecular Systems Biology. 18(9), e10490.","apa":"Angermayr, A., Pang, T. Y., Chevereau, G., Mitosch, K., Lercher, M. J., &#38; Bollenbach, M. T. (2022). Growth‐mediated negative feedback shapes quantitative antibiotic response. <i>Molecular Systems Biology</i>. Embo Press. <a href=\"https://doi.org/10.15252/msb.202110490\">https://doi.org/10.15252/msb.202110490</a>","mla":"Angermayr, Andreas, et al. “Growth‐mediated Negative Feedback Shapes Quantitative Antibiotic Response.” <i>Molecular Systems Biology</i>, vol. 18, no. 9, e10490, Embo Press, 2022, doi:<a href=\"https://doi.org/10.15252/msb.202110490\">10.15252/msb.202110490</a>.","ama":"Angermayr A, Pang TY, Chevereau G, Mitosch K, Lercher MJ, Bollenbach MT. Growth‐mediated negative feedback shapes quantitative antibiotic response. <i>Molecular Systems Biology</i>. 2022;18(9). doi:<a href=\"https://doi.org/10.15252/msb.202110490\">10.15252/msb.202110490</a>","short":"A. Angermayr, T.Y. Pang, G. Chevereau, K. Mitosch, M.J. Lercher, M.T. Bollenbach, Molecular Systems Biology 18 (2022)."},"quality_controlled":"1","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"has_accepted_license":"1","doi":"10.15252/msb.202110490","acknowledged_ssus":[{"_id":"M-Shop"}],"publication_identifier":{"eissn":["1744-4292"]},"date_updated":"2025-06-11T14:10:18Z","external_id":{"pmid":["36124745"],"isi":["000856482800001"]},"oa":1,"month":"09","article_type":"original","file":[{"file_id":"12446","content_type":"application/pdf","success":1,"file_size":1098812,"date_created":"2023-01-30T09:49:55Z","creator":"dernst","checksum":"8b1d8f5ea20c8408acf466435fb6ae01","file_name":"2022_MolecularSystemsBio_Angermayr.pdf","relation":"main_file","date_updated":"2023-01-30T09:49:55Z","access_level":"open_access"}],"_id":"12261","abstract":[{"text":"Dose–response relationships are a general concept for quantitatively describing biological systems across multiple scales, from the molecular to the whole-cell level. A clinically relevant example is the bacterial growth response to antibiotics, which is routinely characterized by dose–response curves. The shape of the dose–response curve varies drastically between antibiotics and plays a key role in treatment, drug interactions, and resistance evolution. However, the mechanisms shaping the dose–response curve remain largely unclear. Here, we show in Escherichia coli that the distinctively shallow dose–response curve of the antibiotic trimethoprim is caused by a negative growth-mediated feedback loop: Trimethoprim slows growth, which in turn weakens the effect of this antibiotic. At the molecular level, this feedback is caused by the upregulation of the drug target dihydrofolate reductase (FolA/DHFR). We show that this upregulation is not a specific response to trimethoprim but follows a universal trend line that depends primarily on the growth rate, irrespective of its cause. Rewiring the feedback loop alters the dose–response curve in a predictable manner, which we corroborate using a mathematical model of cellular resource allocation and growth. Our results indicate that growth-mediated feedback loops may shape drug responses more generally and could be exploited to design evolutionary traps that enable selection against drug resistance.","lang":"eng"}],"intvolume":"        18","publication":"Molecular Systems Biology","department":[{"_id":"ToBo"}],"keyword":["Applied Mathematics","Computational Theory and Mathematics","General Agricultural and Biological Sciences","General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","Information Systems"],"volume":18},{"publication_status":"published","publisher":"eLife Sciences Publications","date_created":"2023-01-16T10:04:15Z","status":"public","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).","project":[{"grant_number":"692692","name":"Biophysics and circuit function of a giant cortical glutamatergic synapse","call_identifier":"H2020","_id":"25B7EB9E-B435-11E9-9278-68D0E5697425"},{"call_identifier":"H2020","_id":"2634E9D2-B435-11E9-9278-68D0E5697425","grant_number":"756502","name":"Circuits of Visual Attention"},{"grant_number":"Z00312","name":"Synaptic communication in neuronal microcircuits","_id":"25C5A090-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"},{"_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","name":"Connecting sensory with motor processing in the superior colliculus","grant_number":"ALTF 1098-2017"}],"year":"2022","author":[{"orcid":"0000-0002-4792-1881","last_name":"Sumser","id":"3320A096-F248-11E8-B48F-1D18A9856A87","first_name":"Anton L","full_name":"Sumser, Anton L"},{"id":"2BD278E6-F248-11E8-B48F-1D18A9856A87","last_name":"Jösch","first_name":"Maximilian A","full_name":"Jösch, Maximilian A","orcid":"0000-0002-3937-1330"},{"last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","first_name":"Peter M","full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804"},{"last_name":"Ben Simon","id":"43DF3136-F248-11E8-B48F-1D18A9856A87","full_name":"Ben Simon, Yoav","first_name":"Yoav"}],"pmid":1,"ec_funded":1,"oa_version":"Published Version","title":"Fast, high-throughput production of improved rabies viral vectors for specific, efficient and versatile transsynaptic retrograde labeling","article_processing_charge":"No","type":"journal_article","day":"15","ddc":["570"],"language":[{"iso":"eng"}],"isi":1,"scopus_import":"1","date_published":"2022-09-15T00:00:00Z","doi":"10.7554/elife.79848","has_accepted_license":"1","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"publication_identifier":{"eissn":["2050-084X"]},"acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"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. <i>eLife</i>. 2022;11. doi:<a href=\"https://doi.org/10.7554/elife.79848\">10.7554/elife.79848</a>","short":"A.L. Sumser, M.A. Jösch, P.M. Jonas, Y. Ben Simon, ELife 11 (2022).","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,” <i>eLife</i>, vol. 11. eLife Sciences Publications, 2022.","apa":"Sumser, A. L., Jösch, M. A., Jonas, P. M., &#38; Ben Simon, Y. (2022). Fast, high-throughput production of improved rabies viral vectors for specific, efficient and versatile transsynaptic retrograde labeling. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.79848\">https://doi.org/10.7554/elife.79848</a>","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.” <i>ELife</i>, vol. 11, 79848, eLife Sciences Publications, 2022, doi:<a href=\"https://doi.org/10.7554/elife.79848\">10.7554/elife.79848</a>.","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.” <i>ELife</i>. eLife Sciences Publications, 2022. <a href=\"https://doi.org/10.7554/elife.79848\">https://doi.org/10.7554/elife.79848</a>."},"file_date_updated":"2023-01-30T11:50:53Z","article_number":"79848","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","quality_controlled":"1","intvolume":"        11","_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."}],"file":[{"creator":"dernst","checksum":"5a2a65e3e7225090c3d8199f3bbd7b7b","file_id":"12463","date_created":"2023-01-30T11:50:53Z","file_size":8506811,"success":1,"content_type":"application/pdf","relation":"main_file","date_updated":"2023-01-30T11:50:53Z","access_level":"open_access","file_name":"2022_eLife_Sumser.pdf"}],"month":"09","article_type":"original","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"volume":11,"department":[{"_id":"MaJö"},{"_id":"PeJo"}],"publication":"eLife","external_id":{"pmid":["36040301"],"isi":["000892204300001"]},"date_updated":"2025-04-15T08:29:05Z","oa":1,"corr_author":"1"},{"external_id":{"isi":["000763891900001"],"pmid":["35241807"]},"date_updated":"2023-08-02T14:41:44Z","department":[{"_id":"CaGu"}],"publication":"Nature Reviews Microbiology","volume":20,"keyword":["General Immunology and Microbiology","Microbiology","Infectious Diseases"],"article_type":"review","month":"08","abstract":[{"lang":"eng","text":"Several promising strategies based on combining or cycling different antibiotics have been proposed to increase efficacy and counteract resistance evolution, but we still lack a deep understanding of the physiological responses and genetic mechanisms that underlie antibiotic interactions and the clinical applicability of these strategies. In antibiotic-exposed bacteria, the combined effects of physiological stress responses and emerging resistance mutations (occurring at different time scales) generate complex and often unpredictable dynamics. In this Review, we present our current understanding of bacterial cell physiology and genetics of responses to antibiotics. We emphasize recently discovered mechanisms of synergistic and antagonistic drug interactions, hysteresis in temporal interactions between antibiotics that arise from microbial physiology and interactions between antibiotics and resistance mutations that can cause collateral sensitivity or cross-resistance. We discuss possible connections between the different phenomena and indicate relevant research directions. A better and more unified understanding of drug and genetic interactions is likely to advance antibiotic therapy."}],"_id":"10812","intvolume":"        20","quality_controlled":"1","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"ieee":"R. Römhild, M. T. Bollenbach, and D. I. Andersson, “The physiology and genetics of bacterial responses to antibiotic combinations,” <i>Nature Reviews Microbiology</i>, vol. 20. Springer Nature, pp. 478–490, 2022.","apa":"Römhild, R., Bollenbach, M. T., &#38; Andersson, D. I. (2022). The physiology and genetics of bacterial responses to antibiotic combinations. <i>Nature Reviews Microbiology</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s41579-022-00700-5\">https://doi.org/10.1038/s41579-022-00700-5</a>","mla":"Römhild, Roderich, et al. “The Physiology and Genetics of Bacterial Responses to Antibiotic Combinations.” <i>Nature Reviews Microbiology</i>, vol. 20, Springer Nature, 2022, pp. 478–90, doi:<a href=\"https://doi.org/10.1038/s41579-022-00700-5\">10.1038/s41579-022-00700-5</a>.","ista":"Römhild R, Bollenbach MT, Andersson DI. 2022. The physiology and genetics of bacterial responses to antibiotic combinations. Nature Reviews Microbiology. 20, 478–490.","chicago":"Römhild, Roderich, Mark Tobias Bollenbach, and Dan I. Andersson. “The Physiology and Genetics of Bacterial Responses to Antibiotic Combinations.” <i>Nature Reviews Microbiology</i>. Springer Nature, 2022. <a href=\"https://doi.org/10.1038/s41579-022-00700-5\">https://doi.org/10.1038/s41579-022-00700-5</a>.","ama":"Römhild R, Bollenbach MT, Andersson DI. The physiology and genetics of bacterial responses to antibiotic combinations. <i>Nature Reviews Microbiology</i>. 2022;20:478-490. doi:<a href=\"https://doi.org/10.1038/s41579-022-00700-5\">10.1038/s41579-022-00700-5</a>","short":"R. Römhild, M.T. Bollenbach, D.I. Andersson, Nature Reviews Microbiology 20 (2022) 478–490."},"publication_identifier":{"issn":["1740-1526"],"eissn":["1740-1534"]},"doi":"10.1038/s41579-022-00700-5","date_published":"2022-08-01T00:00:00Z","scopus_import":"1","language":[{"iso":"eng"}],"isi":1,"type":"journal_article","page":"478-490","day":"01","oa_version":"None","article_processing_charge":"No","title":"The physiology and genetics of bacterial responses to antibiotic combinations","pmid":1,"year":"2022","author":[{"orcid":"0000-0001-9480-5261","full_name":"Römhild, Roderich","first_name":"Roderich","last_name":"Römhild","id":"68E56E44-62B0-11EA-B963-444F3DDC885E"},{"full_name":"Bollenbach, Mark Tobias","first_name":"Mark Tobias","last_name":"Bollenbach","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4398-476X"},{"full_name":"Andersson, Dan I.","first_name":"Dan I.","last_name":"Andersson"}],"status":"public","date_created":"2022-03-04T04:33:49Z","acknowledgement":"The authors thank B. Kavčič and H. Schulenburg for constructive feedback on the manuscript.","publisher":"Springer Nature","publication_status":"published"},{"acknowledged_ssus":[{"_id":"LifeSc"},{"_id":"Bio"}],"publication_identifier":{"issn":["2050-084X"]},"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"doi":"10.7554/elife.75842","has_accepted_license":"1","quality_controlled":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file_date_updated":"2022-06-20T07:44:19Z","citation":{"ieee":"L. Gonzalez Somermeyer <i>et al.</i>, “Heterogeneity of the GFP fitness landscape and data-driven protein design,” <i>eLife</i>, vol. 11. eLife Sciences Publications, 2022.","apa":"Gonzalez Somermeyer, L., Fleiss, A., Mishin, A. S., Bozhanova, N. G., Igolkina, A. A., Meiler, J., … Kondrashov, F. (2022). Heterogeneity of the GFP fitness landscape and data-driven protein design. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.75842\">https://doi.org/10.7554/elife.75842</a>","mla":"Gonzalez Somermeyer, Louisa, et al. “Heterogeneity of the GFP Fitness Landscape and Data-Driven Protein Design.” <i>ELife</i>, vol. 11, 75842, eLife Sciences Publications, 2022, doi:<a href=\"https://doi.org/10.7554/elife.75842\">10.7554/elife.75842</a>.","ista":"Gonzalez Somermeyer L, Fleiss A, Mishin AS, Bozhanova NG, Igolkina AA, Meiler J, Alaball Pujol M-E, Putintseva EV, Sarkisyan KS, Kondrashov F. 2022. Heterogeneity of the GFP fitness landscape and data-driven protein design. eLife. 11, 75842.","chicago":"Gonzalez Somermeyer, Louisa, Aubin Fleiss, Alexander S Mishin, Nina G Bozhanova, Anna A Igolkina, Jens Meiler, Maria-Elisenda Alaball Pujol, Ekaterina V Putintseva, Karen S Sarkisyan, and Fyodor Kondrashov. “Heterogeneity of the GFP Fitness Landscape and Data-Driven Protein Design.” <i>ELife</i>. eLife Sciences Publications, 2022. <a href=\"https://doi.org/10.7554/elife.75842\">https://doi.org/10.7554/elife.75842</a>.","ama":"Gonzalez Somermeyer L, Fleiss A, Mishin AS, et al. Heterogeneity of the GFP fitness landscape and data-driven protein design. <i>eLife</i>. 2022;11. doi:<a href=\"https://doi.org/10.7554/elife.75842\">10.7554/elife.75842</a>","short":"L. Gonzalez Somermeyer, A. Fleiss, A.S. Mishin, N.G. Bozhanova, A.A. Igolkina, J. Meiler, M.-E. Alaball Pujol, E.V. Putintseva, K.S. Sarkisyan, F. Kondrashov, ELife 11 (2022)."},"article_number":"75842","department":[{"_id":"GradSch"},{"_id":"FyKo"}],"publication":"eLife","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"volume":11,"article_type":"original","month":"05","abstract":[{"text":"Studies of protein fitness landscapes reveal biophysical constraints guiding protein evolution and empower prediction of functional proteins. However, generalisation of these findings is limited due to scarceness of systematic data on fitness landscapes of proteins with a defined evolutionary relationship. We characterized the fitness peaks of four orthologous fluorescent proteins with a broad range of sequence divergence. While two of the four studied fitness peaks were sharp, the other two were considerably flatter, being almost entirely free of epistatic interactions. Mutationally robust proteins, characterized by a flat fitness peak, were not optimal templates for machine-learning-driven protein design – instead, predictions were more accurate for fragile proteins with epistatic landscapes. Our work paves insights for practical application of fitness landscape heterogeneity in protein engineering.","lang":"eng"}],"_id":"11448","intvolume":"        11","file":[{"creator":"dernst","checksum":"7573c28f44028ab0cc81faef30039e44","file_id":"11454","content_type":"application/pdf","success":1,"file_size":5297213,"date_created":"2022-06-20T07:44:19Z","relation":"main_file","access_level":"open_access","date_updated":"2022-06-20T07:44:19Z","file_name":"2022_eLife_Somermeyer.pdf"}],"oa":1,"corr_author":"1","external_id":{"isi":["000799197200001"],"pmid":["35510622"]},"related_material":{"record":[{"status":"public","relation":"dissertation_contains","id":"17850"}],"link":[{"relation":"software","url":"https://github.com/aequorea238/Orthologous_GFP_Fitness_Peaks"}]},"date_updated":"2026-04-07T13:25:01Z","project":[{"name":"Characterizing the fitness landscape on population and global scales","grant_number":"771209","_id":"26580278-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"name":"International IST Doctoral Program","grant_number":"665385","call_identifier":"H2020","_id":"2564DBCA-B435-11E9-9278-68D0E5697425"}],"date_created":"2022-06-18T09:06:59Z","status":"public","acknowledgement":"We thank Ondřej Draganov, Rodrigo Redondo, Bor Kavčič, Mia Juračić and Andrea Pauli for discussion and technical advice. We thank Anita Testa Salmazo for advice on resin protein purification, Dmitry Bolotin and the Milaboratory (milaboratory.com) for access to computing and storage infrastructure, and Josef Houser and Eva Fujdiarova for technical assistance and data interpretation. Core facility Biomolecular Interactions and Crystallization of CEITEC Masaryk University is gratefully acknowledged for the obtaining of the scientific data presented in this paper. This research was supported by the Scientific Service Units (SSU) of IST-Austria\r\nthrough resources provided by the Bioimaging Facility (BIF), and the Life Science Facility (LSF). MiSeq and HiSeq NGS sequencing was performed by the Next Generation Sequencing Facility at Vienna BioCenter Core Facilities (VBCF), member of the Vienna BioCenter (VBC), Austria. FACS was performed at the BioOptics Facility of the Institute of Molecular Pathology (IMP), Austria. We also thank the Biomolecular Crystallography Facility in the Vanderbilt University Center for Structural Biology. We are grateful to Joel M Harp for help with X-ray data collection. This work was supported by the ERC Consolidator grant to FAK (771209—CharFL). KSS acknowledges support by President’s Grant МК–5405.2021.1.4, the Imperial College Research Fellowship and the MRC London Institute of Medical Sciences (UKRI MC-A658-5QEA0).\r\nAF is supported by the Marie Skłodowska-Curie Fellowship (H2020-MSCA-IF-2019, Grant Agreement No. 898203, Project acronym \"FLINDIP\"). Experiments were partially carried out using equipment provided by the Institute of Bioorganic Chemistry of the Russian Academy of Sciences Сore Facility (CKP IBCH). This work was supported by a Russian Science Foundation grant 19-74-10102.This project has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie Grant Agreement No. 665,385.","publisher":"eLife Sciences Publications","publication_status":"published","oa_version":"Published Version","ec_funded":1,"article_processing_charge":"No","title":"Heterogeneity of the GFP fitness landscape and data-driven protein design","pmid":1,"year":"2022","author":[{"last_name":"Gonzalez Somermeyer","id":"4720D23C-F248-11E8-B48F-1D18A9856A87","full_name":"Gonzalez Somermeyer, Louisa","first_name":"Louisa","orcid":"0000-0001-9139-5383"},{"last_name":"Fleiss","first_name":"Aubin","full_name":"Fleiss, Aubin"},{"first_name":"Alexander S","full_name":"Mishin, Alexander S","last_name":"Mishin"},{"full_name":"Bozhanova, Nina G","first_name":"Nina G","last_name":"Bozhanova"},{"last_name":"Igolkina","first_name":"Anna A","full_name":"Igolkina, Anna A"},{"full_name":"Meiler, Jens","first_name":"Jens","last_name":"Meiler"},{"full_name":"Alaball Pujol, Maria-Elisenda","first_name":"Maria-Elisenda","last_name":"Alaball Pujol"},{"first_name":"Ekaterina V","full_name":"Putintseva, Ekaterina V","last_name":"Putintseva"},{"last_name":"Sarkisyan","first_name":"Karen S","full_name":"Sarkisyan, Karen S"},{"id":"44FDEF62-F248-11E8-B48F-1D18A9856A87","last_name":"Kondrashov","first_name":"Fyodor","full_name":"Kondrashov, Fyodor","orcid":"0000-0001-8243-4694"}],"scopus_import":"1","language":[{"iso":"eng"}],"isi":1,"type":"journal_article","ddc":["570"],"day":"05","date_published":"2022-05-05T00:00:00Z"},{"doi":"10.15252/embj.2021107711","publication_identifier":{"issn":["0261-4189"],"eissn":["1460-2075"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","main_file_link":[{"open_access":"1","url":"https://doi.org/10.15252/embj.2021107711"}],"citation":{"ama":"Geiger F, Acker J, Papa G, et al. Liquid–liquid phase separation underpins the formation of replication factories in rotaviruses. <i>The EMBO Journal</i>. 2021;40(21). doi:<a href=\"https://doi.org/10.15252/embj.2021107711\">10.15252/embj.2021107711</a>","short":"F. Geiger, J. Acker, G. Papa, X. Wang, W.E. Arter, K.L. Saar, N.A. Erkamp, R. Qi, J.P.K. Bravo, S. Strauss, G. Krainer, O.R. Burrone, R. Jungmann, T.P. Knowles, H. Engelke, A. Borodavka, The EMBO Journal 40 (2021).","ieee":"F. Geiger <i>et al.</i>, “Liquid–liquid phase separation underpins the formation of replication factories in rotaviruses,” <i>The EMBO Journal</i>, vol. 40, no. 21. Embo Press, 2021.","apa":"Geiger, F., Acker, J., Papa, G., Wang, X., Arter, W. E., Saar, K. L., … Borodavka, A. (2021). Liquid–liquid phase separation underpins the formation of replication factories in rotaviruses. <i>The EMBO Journal</i>. Embo Press. <a href=\"https://doi.org/10.15252/embj.2021107711\">https://doi.org/10.15252/embj.2021107711</a>","mla":"Geiger, Florian, et al. “Liquid–Liquid Phase Separation Underpins the Formation of Replication Factories in Rotaviruses.” <i>The EMBO Journal</i>, vol. 40, no. 21, e107711, Embo Press, 2021, doi:<a href=\"https://doi.org/10.15252/embj.2021107711\">10.15252/embj.2021107711</a>.","ista":"Geiger F, Acker J, Papa G, Wang X, Arter WE, Saar KL, Erkamp NA, Qi R, Bravo JPK, Strauss S, Krainer G, Burrone OR, Jungmann R, Knowles TP, Engelke H, Borodavka A. 2021. Liquid–liquid phase separation underpins the formation of replication factories in rotaviruses. The EMBO Journal. 40(21), e107711.","chicago":"Geiger, Florian, Julia Acker, Guido Papa, Xinyu Wang, William E Arter, Kadi L Saar, Nadia A Erkamp, et al. “Liquid–Liquid Phase Separation Underpins the Formation of Replication Factories in Rotaviruses.” <i>The EMBO Journal</i>. Embo Press, 2021. <a href=\"https://doi.org/10.15252/embj.2021107711\">https://doi.org/10.15252/embj.2021107711</a>."},"article_number":"e107711","quality_controlled":"1","month":"11","article_type":"original","intvolume":"        40","_id":"15138","abstract":[{"text":"RNA viruses induce the formation of subcellular organelles that provide microenvironments conducive to their replication. Here we show that replication factories of rotaviruses represent protein‐RNA condensates that are formed via liquid–liquid phase separation of the viroplasm‐forming proteins NSP5 and rotavirus RNA chaperone NSP2. Upon mixing, these proteins readily form condensates at physiologically relevant low micromolar concentrations achieved in the cytoplasm of virus‐infected cells. Early infection stage condensates could be reversibly dissolved by 1,6‐hexanediol, as well as propylene glycol that released rotavirus transcripts from these condensates. During the early stages of infection, propylene glycol treatments reduced viral replication and phosphorylation of the condensate‐forming protein NSP5. During late infection, these condensates exhibited altered material properties and became resistant to propylene glycol, coinciding with hyperphosphorylation of NSP5. Some aspects of the assembly of cytoplasmic rotavirus replication factories mirror the formation of other ribonucleoprotein granules. Such viral RNA‐rich condensates that support replication of multi‐segmented genomes represent an attractive target for developing novel therapeutic approaches.","lang":"eng"}],"publication":"The EMBO Journal","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","Molecular Biology","General Neuroscience"],"volume":40,"external_id":{"pmid":["34524703"]},"date_updated":"2024-06-04T06:08:16Z","oa":1,"extern":"1","publisher":"Embo Press","publication_status":"published","date_created":"2024-03-20T10:42:39Z","status":"public","year":"2021","author":[{"last_name":"Geiger","first_name":"Florian","full_name":"Geiger, Florian"},{"full_name":"Acker, Julia","first_name":"Julia","last_name":"Acker"},{"first_name":"Guido","full_name":"Papa, Guido","last_name":"Papa"},{"last_name":"Wang","full_name":"Wang, Xinyu","first_name":"Xinyu"},{"last_name":"Arter","full_name":"Arter, William E","first_name":"William E"},{"first_name":"Kadi L","full_name":"Saar, Kadi L","last_name":"Saar"},{"first_name":"Nadia A","full_name":"Erkamp, Nadia A","last_name":"Erkamp"},{"first_name":"Runzhang","full_name":"Qi, Runzhang","last_name":"Qi"},{"orcid":"0000-0003-0456-0753","last_name":"Bravo","id":"96aecfa5-8931-11ee-af30-aa6a5d6eee0e","first_name":"Jack Peter Kelly","full_name":"Bravo, Jack Peter Kelly"},{"first_name":"Sebastian","full_name":"Strauss, Sebastian","last_name":"Strauss"},{"last_name":"Krainer","full_name":"Krainer, Georg","first_name":"Georg"},{"last_name":"Burrone","full_name":"Burrone, Oscar R","first_name":"Oscar R"},{"full_name":"Jungmann, Ralf","first_name":"Ralf","last_name":"Jungmann"},{"last_name":"Knowles","first_name":"Tuomas PJ","full_name":"Knowles, Tuomas PJ"},{"last_name":"Engelke","full_name":"Engelke, Hanna","first_name":"Hanna"},{"last_name":"Borodavka","first_name":"Alexander","full_name":"Borodavka, Alexander"}],"oa_version":"Published Version","title":"Liquid–liquid phase separation underpins the formation of replication factories in rotaviruses","article_processing_charge":"Yes","pmid":1,"type":"journal_article","day":"02","scopus_import":"1","language":[{"iso":"eng"}],"date_published":"2021-11-02T00:00:00Z","issue":"21"},{"status":"public","date_created":"2024-04-03T07:58:11Z","publication_status":"published","publisher":"eLife Sciences Publications","pmid":1,"article_processing_charge":"Yes","title":"Incomplete removal of extracellular glutamate controls synaptic transmission and integration at a cerebellar synapse","oa_version":"Published Version","author":[{"last_name":"Balmer","full_name":"Balmer, Timothy S","first_name":"Timothy S"},{"orcid":"0000-0003-0005-401X","last_name":"Borges Merjane","id":"4305C450-F248-11E8-B48F-1D18A9856A87","first_name":"Carolina","full_name":"Borges Merjane, Carolina"},{"first_name":"Laurence O","full_name":"Trussell, Laurence O","last_name":"Trussell"}],"year":"2021","language":[{"iso":"eng"}],"day":"22","ddc":["570"],"type":"journal_article","date_published":"2021-02-22T00:00:00Z","publication_identifier":{"issn":["2050-084X"]},"has_accepted_license":"1","doi":"10.7554/elife.63819","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"quality_controlled":"1","article_number":"e63819","citation":{"mla":"Balmer, Timothy S., et al. “Incomplete Removal of Extracellular Glutamate Controls Synaptic Transmission and Integration at a Cerebellar Synapse.” <i>ELife</i>, vol. 10, e63819, eLife Sciences Publications, 2021, doi:<a href=\"https://doi.org/10.7554/elife.63819\">10.7554/elife.63819</a>.","apa":"Balmer, T. S., Borges Merjane, C., &#38; Trussell, L. O. (2021). Incomplete removal of extracellular glutamate controls synaptic transmission and integration at a cerebellar synapse. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.63819\">https://doi.org/10.7554/elife.63819</a>","ista":"Balmer TS, Borges Merjane C, Trussell LO. 2021. Incomplete removal of extracellular glutamate controls synaptic transmission and integration at a cerebellar synapse. eLife. 10, e63819.","chicago":"Balmer, Timothy S, Carolina Borges Merjane, and Laurence O Trussell. “Incomplete Removal of Extracellular Glutamate Controls Synaptic Transmission and Integration at a Cerebellar Synapse.” <i>ELife</i>. eLife Sciences Publications, 2021. <a href=\"https://doi.org/10.7554/elife.63819\">https://doi.org/10.7554/elife.63819</a>.","ieee":"T. S. Balmer, C. Borges Merjane, and L. O. Trussell, “Incomplete removal of extracellular glutamate controls synaptic transmission and integration at a cerebellar synapse,” <i>eLife</i>, vol. 10. eLife Sciences Publications, 2021.","short":"T.S. Balmer, C. Borges Merjane, L.O. Trussell, ELife 10 (2021).","ama":"Balmer TS, Borges Merjane C, Trussell LO. Incomplete removal of extracellular glutamate controls synaptic transmission and integration at a cerebellar synapse. <i>eLife</i>. 2021;10. doi:<a href=\"https://doi.org/10.7554/elife.63819\">10.7554/elife.63819</a>"},"file_date_updated":"2024-04-09T11:13:07Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","volume":10,"keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"publication":"eLife","department":[{"_id":"PeJo"}],"file":[{"content_type":"application/pdf","date_created":"2024-04-09T11:13:07Z","file_size":6997954,"success":1,"file_id":"15307","checksum":"bbd4de2e54b7fbc11fba14f59e87fe3f","creator":"dernst","file_name":"2021_eLife_Balmer.pdf","access_level":"open_access","date_updated":"2024-04-09T11:13:07Z","relation":"main_file"}],"_id":"15273","abstract":[{"lang":"eng","text":"Synapses of glutamatergic mossy fibers (MFs) onto cerebellar unipolar brush cells (UBCs) generate slow excitatory (ON) or inhibitory (OFF) postsynaptic responses dependent on the complement of glutamate receptors expressed on the UBC’s large dendritic brush. Using mouse brain slice recording and computational modeling of synaptic transmission, we found that substantial glutamate is maintained in the UBC synaptic cleft, sufficient to modify spontaneous firing in OFF UBCs and tonically desensitize AMPARs of ON UBCs. The source of this ambient glutamate was spontaneous, spike-independent exocytosis from the MF terminal, and its level was dependent on activity of glutamate transporters EAAT1–2. Increasing levels of ambient glutamate shifted the polarity of evoked synaptic responses in ON UBCs and altered the phase of responses to in vivo-like synaptic activity. Unlike classical fast synapses, receptors at the UBC synapse are virtually always exposed to a significant level of glutamate, which varies in a graded manner during transmission."}],"intvolume":"        10","article_type":"original","month":"02","oa":1,"date_updated":"2024-04-09T11:15:01Z","external_id":{"pmid":["33616036"]}},{"oa":1,"date_updated":"2024-10-21T06:02:05Z","external_id":{"isi":["000720945900001"]},"publication":"eLife","department":[{"_id":"GaNo"}],"volume":10,"keyword":["general immunology and microbiology","general biochemistry","genetics and molecular biology","general medicine","general neuroscience"],"article_type":"original","month":"11","file":[{"creator":"lgarciar","checksum":"59318e9e41507cec83c2f4070e6ad540","file_id":"10302","success":1,"date_created":"2021-11-18T07:02:02Z","file_size":2477302,"content_type":"application/pdf","relation":"main_file","date_updated":"2021-11-18T07:02:02Z","access_level":"open_access","file_name":"elife-71575-v1.pdf"}],"abstract":[{"lang":"eng","text":"De novo protein synthesis is required for synapse modifications underlying stable memory encoding. Yet neurons are highly compartmentalized cells and how protein synthesis can be regulated at the synapse level is unknown. Here, we characterize neuronal signaling complexes formed by the postsynaptic scaffold GIT1, the mechanistic target of rapamycin (mTOR) kinase, and Raptor that couple synaptic stimuli to mTOR-dependent protein synthesis; and identify NMDA receptors containing GluN3A subunits as key negative regulators of GIT1 binding to mTOR. Disruption of GIT1/mTOR complexes by enhancing GluN3A expression or silencing GIT1 inhibits synaptic mTOR activation and restricts the mTOR-dependent translation of specific activity-regulated mRNAs. Conversely, GluN3A removal enables complex formation, potentiates mTOR-dependent protein synthesis, and facilitates the consolidation of associative and spatial memories in mice. The memory enhancement becomes evident with light or spaced training, can be achieved by selectively deleting GluN3A from excitatory neurons during adulthood, and does not compromise other aspects of cognition such as memory flexibility or extinction. Our findings provide mechanistic insight into synaptic translational control and reveal a potentially selective target for cognitive enhancement."}],"_id":"10301","intvolume":"        10","quality_controlled":"1","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","article_number":"e71575","citation":{"ama":"Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, et al. Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly. <i>eLife</i>. 2021;10. doi:<a href=\"https://doi.org/10.7554/elife.71575\">10.7554/elife.71575</a>","short":"M.J. Conde-Dusman, P.N. Dey, Ó. Elía-Zudaire, L.E. Garcia Rabaneda, C. García-Lira, T. Grand, V. Briz, E.R. Velasco, R. Andero Galí, S. Niñerola, A. Barco, P. Paoletti, J.F. Wesseling, F. Gardoni, S.J. Tavalin, I. Perez-Otaño, ELife 10 (2021).","ieee":"M. J. Conde-Dusman <i>et al.</i>, “Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly,” <i>eLife</i>, vol. 10. eLife Sciences Publications, 2021.","chicago":"Conde-Dusman, María J, Partha N Dey, Óscar Elía-Zudaire, Luis E Garcia Rabaneda, Carmen García-Lira, Teddy Grand, Victor Briz, et al. “Control of Protein Synthesis and Memory by GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1 Assembly.” <i>ELife</i>. eLife Sciences Publications, 2021. <a href=\"https://doi.org/10.7554/elife.71575\">https://doi.org/10.7554/elife.71575</a>.","mla":"Conde-Dusman, María J., et al. “Control of Protein Synthesis and Memory by GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1 Assembly.” <i>ELife</i>, vol. 10, e71575, eLife Sciences Publications, 2021, doi:<a href=\"https://doi.org/10.7554/elife.71575\">10.7554/elife.71575</a>.","ista":"Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, Garcia Rabaneda LE, García-Lira C, Grand T, Briz V, Velasco ER, Andero Galí R, Niñerola S, Barco A, Paoletti P, Wesseling JF, Gardoni F, Tavalin SJ, Perez-Otaño I. 2021. Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly. eLife. 10, e71575.","apa":"Conde-Dusman, M. J., Dey, P. N., Elía-Zudaire, Ó., Garcia Rabaneda, L. E., García-Lira, C., Grand, T., … Perez-Otaño, I. (2021). Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.71575\">https://doi.org/10.7554/elife.71575</a>"},"file_date_updated":"2021-11-18T07:02:02Z","publication_identifier":{"issn":["2050-084X"]},"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"has_accepted_license":"1","doi":"10.7554/elife.71575","date_published":"2021-11-17T00:00:00Z","scopus_import":"1","isi":1,"language":[{"iso":"eng"}],"ddc":["570"],"day":"17","type":"journal_article","article_processing_charge":"No","title":"Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly","oa_version":"Published Version","author":[{"first_name":"María J","full_name":"Conde-Dusman, María J","last_name":"Conde-Dusman"},{"first_name":"Partha N","full_name":"Dey, Partha N","last_name":"Dey"},{"first_name":"Óscar","full_name":"Elía-Zudaire, Óscar","last_name":"Elía-Zudaire"},{"last_name":"Garcia Rabaneda","id":"33D1B084-F248-11E8-B48F-1D18A9856A87","full_name":"Garcia Rabaneda, Luis E","first_name":"Luis E"},{"last_name":"García-Lira","first_name":"Carmen","full_name":"García-Lira, Carmen"},{"last_name":"Grand","full_name":"Grand, Teddy","first_name":"Teddy"},{"last_name":"Briz","full_name":"Briz, Victor","first_name":"Victor"},{"first_name":"Eric R","full_name":"Velasco, Eric R","last_name":"Velasco"},{"first_name":"Raül","full_name":"Andero Galí, Raül","last_name":"Andero Galí"},{"first_name":"Sergio","full_name":"Niñerola, Sergio","last_name":"Niñerola"},{"last_name":"Barco","full_name":"Barco, Angel","first_name":"Angel"},{"full_name":"Paoletti, Pierre","first_name":"Pierre","last_name":"Paoletti"},{"last_name":"Wesseling","full_name":"Wesseling, John F","first_name":"John F"},{"last_name":"Gardoni","first_name":"Fabrizio","full_name":"Gardoni, Fabrizio"},{"first_name":"Steven J","full_name":"Tavalin, Steven J","last_name":"Tavalin"},{"last_name":"Perez-Otaño","full_name":"Perez-Otaño, Isabel","first_name":"Isabel"}],"year":"2021","acknowledgement":"We thank Stuart Lipton and Nobuki Nakanishi for providing the Grin3a knockout mice, Beverly Davidson for the AAV-caRheb, Jose Esteban for help with behavioral and biochemical experiments, and Noelia Campillo, Rebeca Martínez-Turrillas, and Ana Navarro for expert technical help. Work was funded by the UTE project CIMA; fellowships from the Fundación Tatiana Pérez de Guzmán el Bueno, FEBS, and IBRO (to M.J.C.D.), Generalitat Valenciana (to O.E.-Z.), Juan de la Cierva (to L.G.R.), FPI-MINECO (to E.R.V., to S.N.) and Intertalentum postdoctoral program (to V.B.); ANR (GluBrain3A) and ERC Advanced Grants (#693021) (to P.P.); Ramón y Cajal program RYC2014-15784, RETOS-MINECO SAF2016-76565-R, ERANET-Neuron JTC 2019 ISCIII AC19/00077 FEDER funds (to R.A.); RETOS-MINECO SAF2017-87928-R (to A.B.); an NIH grant (NS76637) and UTHSC College of Medicine funds (to S.J.T.); and NARSAD Independent Investigator Award and grants from the MINECO (CSD2008-00005, SAF2013-48983R, SAF2016-80895-R), Generalitat Valenciana (PROMETEO 2019/020)(to I.P.O.) and Severo-Ochoa Excellence Awards (SEV-2013-0317, SEV-2017-0723).","status":"public","date_created":"2021-11-18T06:59:45Z","publisher":"eLife Sciences Publications","publication_status":"published"},{"abstract":[{"lang":"eng","text":"We report the complete analysis of a deterministic model of deleterious mutations and negative selection against them at two haploid loci without recombination. As long as mutation is a weaker force than selection, mutant alleles remain rare at the only stable equilibrium, and otherwise, a variety of dynamics are possible. If the mutation-free genotype is absent, generally the only stable equilibrium is the one that corresponds to fixation of the mutant allele at the locus where it is less deleterious. This result suggests that fixation of a deleterious allele that follows a click of the Muller’s ratchet is governed by natural selection, instead of random drift."}],"_id":"9387","intvolume":"       524","month":"04","article_type":"original","volume":524,"keyword":["General Biochemistry","Genetics and Molecular Biology","Modelling and Simulation","Statistics and Probability","General Immunology and Microbiology","Applied Mathematics","General Agricultural and Biological Sciences","General Medicine"],"publication":"Journal of Theoretical Biology","department":[{"_id":"GradSch"}],"date_updated":"2025-06-12T06:40:55Z","external_id":{"pmid":["33901507"],"isi":["000659161500002"]},"oa":1,"doi":"10.1016/j.jtbi.2021.110729","publication_identifier":{"issn":["0022-5193"]},"article_number":"110729","citation":{"ama":"Khudiakova K, Neretina TY, Kondrashov AS. Two linked loci under mutation-selection balance and Muller’s ratchet. <i>Journal of Theoretical Biology</i>. 2021;524. doi:<a href=\"https://doi.org/10.1016/j.jtbi.2021.110729\">10.1016/j.jtbi.2021.110729</a>","short":"K. Khudiakova, T.Y. Neretina, A.S. Kondrashov, Journal of Theoretical Biology 524 (2021).","ieee":"K. Khudiakova, T. Y. Neretina, and A. S. Kondrashov, “Two linked loci under mutation-selection balance and Muller’s ratchet,” <i>Journal of Theoretical Biology</i>, vol. 524. Elsevier , 2021.","chicago":"Khudiakova, Kseniia, Tatiana Yu. Neretina, and Alexey S. Kondrashov. “Two Linked Loci under Mutation-Selection Balance and Muller’s Ratchet.” <i>Journal of Theoretical Biology</i>. Elsevier , 2021. <a href=\"https://doi.org/10.1016/j.jtbi.2021.110729\">https://doi.org/10.1016/j.jtbi.2021.110729</a>.","apa":"Khudiakova, K., Neretina, T. Y., &#38; Kondrashov, A. S. (2021). Two linked loci under mutation-selection balance and Muller’s ratchet. <i>Journal of Theoretical Biology</i>. Elsevier . <a href=\"https://doi.org/10.1016/j.jtbi.2021.110729\">https://doi.org/10.1016/j.jtbi.2021.110729</a>","ista":"Khudiakova K, Neretina TY, Kondrashov AS. 2021. Two linked loci under mutation-selection balance and Muller’s ratchet. Journal of Theoretical Biology. 524, 110729.","mla":"Khudiakova, Kseniia, et al. “Two Linked Loci under Mutation-Selection Balance and Muller’s Ratchet.” <i>Journal of Theoretical Biology</i>, vol. 524, 110729, Elsevier , 2021, doi:<a href=\"https://doi.org/10.1016/j.jtbi.2021.110729\">10.1016/j.jtbi.2021.110729</a>."},"main_file_link":[{"open_access":"1","url":"https://www.biorxiv.org/content/10.1101/477489v1"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","quality_controlled":"1","day":"24","type":"journal_article","isi":1,"language":[{"iso":"eng"}],"scopus_import":"1","date_published":"2021-04-24T00:00:00Z","publication_status":"published","publisher":"Elsevier ","acknowledgement":"This work was supported by the Russian Science Foundation grant N 16-14-10173.","status":"public","date_created":"2021-05-12T05:58:42Z","author":[{"orcid":"0000-0002-6246-1465","full_name":"Khudiakova, Kseniia","first_name":"Kseniia","last_name":"Khudiakova","id":"4E6DC800-AE37-11E9-AC72-31CAE5697425"},{"full_name":"Neretina, Tatiana Yu.","first_name":"Tatiana Yu.","last_name":"Neretina"},{"last_name":"Kondrashov","first_name":"Alexey S.","full_name":"Kondrashov, Alexey S."}],"year":"2021","pmid":1,"title":"Two linked loci under mutation-selection balance and Muller’s ratchet","article_processing_charge":"No","oa_version":"Preprint"},{"publication":"eLife","volume":9,"keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"month":"02","article_type":"original","_id":"15153","abstract":[{"lang":"eng","text":"Mammalian circadian rhythms are generated by a transcription-based feedback loop in which CLOCK:BMAL1 drives transcription of its repressors (PER1/2, CRY1/2), which ultimately interact with CLOCK:BMAL1 to close the feedback loop with ~24 hr periodicity. Here we pinpoint a key difference between CRY1 and CRY2 that underlies their differential strengths as transcriptional repressors. Both cryptochromes bind the BMAL1 transactivation domain similarly to sequester it from coactivators and repress CLOCK:BMAL1 activity. However, we find that CRY1 is recruited with much higher affinity to the PAS domain core of CLOCK:BMAL1, allowing it to serve as a stronger repressor that lengthens circadian period. We discovered a dynamic serine-rich loop adjacent to the secondary pocket in the photolyase homology region (PHR) domain that regulates differential binding of cryptochromes to the PAS domain core of CLOCK:BMAL1. Notably, binding of the co-repressor PER2 remodels the serine loop of CRY2, making it more CRY1-like and enhancing its affinity for CLOCK:BMAL1."}],"intvolume":"         9","oa":1,"extern":"1","date_updated":"2024-03-25T12:25:02Z","publication_identifier":{"issn":["2050-084X"]},"doi":"10.7554/elife.55275","quality_controlled":"1","main_file_link":[{"open_access":"1","url":"https://doi.org/10.7554/eLife.55275"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_number":"55275","citation":{"ama":"Fribourgh JL, Srivastava A, Sandate CR, et al. Dynamics at the serine loop underlie differential affinity of cryptochromes for CLOCK:BMAL1 to control circadian timing. <i>eLife</i>. 2020;9. doi:<a href=\"https://doi.org/10.7554/elife.55275\">10.7554/elife.55275</a>","short":"J.L. Fribourgh, A. Srivastava, C.R. Sandate, A.K. Michael, P.L. Hsu, C. Rakers, L.T. Nguyen, M.R. Torgrimson, G.C.G. Parico, S. Tripathi, N. Zheng, G.C. Lander, T. Hirota, F. Tama, C.L. Partch, ELife 9 (2020).","ieee":"J. L. Fribourgh <i>et al.</i>, “Dynamics at the serine loop underlie differential affinity of cryptochromes for CLOCK:BMAL1 to control circadian timing,” <i>eLife</i>, vol. 9. eLife Sciences Publications, 2020.","chicago":"Fribourgh, Jennifer L, Ashutosh Srivastava, Colby R Sandate, Alicia K. Michael, Peter L Hsu, Christin Rakers, Leslee T Nguyen, et al. “Dynamics at the Serine Loop Underlie Differential Affinity of Cryptochromes for CLOCK:BMAL1 to Control Circadian Timing.” <i>ELife</i>. eLife Sciences Publications, 2020. <a href=\"https://doi.org/10.7554/elife.55275\">https://doi.org/10.7554/elife.55275</a>.","ista":"Fribourgh JL, Srivastava A, Sandate CR, Michael AK, Hsu PL, Rakers C, Nguyen LT, Torgrimson MR, Parico GCG, Tripathi S, Zheng N, Lander GC, Hirota T, Tama F, Partch CL. 2020. Dynamics at the serine loop underlie differential affinity of cryptochromes for CLOCK:BMAL1 to control circadian timing. eLife. 9, 55275.","apa":"Fribourgh, J. L., Srivastava, A., Sandate, C. R., Michael, A. K., Hsu, P. L., Rakers, C., … Partch, C. L. (2020). Dynamics at the serine loop underlie differential affinity of cryptochromes for CLOCK:BMAL1 to control circadian timing. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.55275\">https://doi.org/10.7554/elife.55275</a>","mla":"Fribourgh, Jennifer L., et al. “Dynamics at the Serine Loop Underlie Differential Affinity of Cryptochromes for CLOCK:BMAL1 to Control Circadian Timing.” <i>ELife</i>, vol. 9, 55275, eLife Sciences Publications, 2020, doi:<a href=\"https://doi.org/10.7554/elife.55275\">10.7554/elife.55275</a>."},"scopus_import":"1","language":[{"iso":"eng"}],"day":"26","type":"journal_article","date_published":"2020-02-26T00:00:00Z","status":"public","date_created":"2024-03-21T07:55:12Z","publisher":"eLife Sciences Publications","publication_status":"published","article_processing_charge":"No","title":"Dynamics at the serine loop underlie differential affinity of cryptochromes for CLOCK:BMAL1 to control circadian timing","oa_version":"Published Version","author":[{"last_name":"Fribourgh","first_name":"Jennifer L","full_name":"Fribourgh, Jennifer L"},{"last_name":"Srivastava","full_name":"Srivastava, Ashutosh","first_name":"Ashutosh"},{"first_name":"Colby R","full_name":"Sandate, Colby R","last_name":"Sandate"},{"first_name":"Alicia Kathleen","full_name":"Michael, Alicia Kathleen","last_name":"Michael","id":"6437c950-2a03-11ee-914d-d6476dd7b75c"},{"last_name":"Hsu","first_name":"Peter L","full_name":"Hsu, Peter L"},{"first_name":"Christin","full_name":"Rakers, Christin","last_name":"Rakers"},{"first_name":"Leslee T","full_name":"Nguyen, Leslee T","last_name":"Nguyen"},{"last_name":"Torgrimson","full_name":"Torgrimson, Megan R","first_name":"Megan R"},{"last_name":"Parico","first_name":"Gian Carlo G","full_name":"Parico, Gian Carlo G"},{"last_name":"Tripathi","first_name":"Sarvind","full_name":"Tripathi, Sarvind"},{"first_name":"Ning","full_name":"Zheng, Ning","last_name":"Zheng"},{"first_name":"Gabriel C","full_name":"Lander, Gabriel C","last_name":"Lander"},{"last_name":"Hirota","full_name":"Hirota, Tsuyoshi","first_name":"Tsuyoshi"},{"full_name":"Tama, Florence","first_name":"Florence","last_name":"Tama"},{"first_name":"Carrie L","full_name":"Partch, Carrie L","last_name":"Partch"}],"year":"2020"},{"publication":"eLife","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"volume":9,"month":"09","article_type":"original","abstract":[{"lang":"eng","text":"Vascular dysfunctions are a common feature of multiple age-related diseases. However, modeling healthy and pathological aging of the human vasculature represents an unresolved experimental challenge. Here, we generated induced vascular endothelial cells (iVECs) and smooth muscle cells (iSMCs) by direct reprogramming of healthy human fibroblasts from donors of different ages and Hutchinson-Gilford Progeria Syndrome (HGPS) patients. iVECs induced from old donors revealed upregulation of GSTM1 and PALD1, genes linked to oxidative stress, inflammation and endothelial junction stability, as vascular aging markers. A functional assay performed on PALD1 KD VECs demonstrated a recovery in vascular permeability. We found that iSMCs from HGPS donors overexpressed bone morphogenetic protein (BMP)−4, which plays a key role in both vascular calcification and endothelial barrier damage observed in HGPS. Strikingly, BMP4 concentrations are higher in serum from HGPS vs. age-matched mice. Furthermore, targeting BMP4 with blocking antibody recovered the functionality of the vascular barrier in vitro, hence representing a potential future therapeutic strategy to limit cardiovascular dysfunction in HGPS. These results show that iVECs and iSMCs retain disease-related signatures, allowing modeling of vascular aging and HGPS in vitro."}],"_id":"11055","intvolume":"         9","file":[{"file_name":"2020_eLife_Bersini.pdf","relation":"main_file","date_updated":"2022-04-08T06:53:10Z","access_level":"open_access","file_id":"11132","date_created":"2022-04-08T06:53:10Z","file_size":4399825,"success":1,"content_type":"application/pdf","creator":"dernst","checksum":"f8b3821349a194050be02570d8fe7d4b"}],"extern":"1","oa":1,"external_id":{"pmid":["32896271"]},"date_updated":"2024-10-14T11:17:02Z","publication_identifier":{"issn":["2050-084X"]},"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"doi":"10.7554/elife.54383","has_accepted_license":"1","quality_controlled":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"ama":"Bersini S, Schulte R, Huang L, Tsai H, Hetzer M. Direct reprogramming of human smooth muscle and vascular endothelial cells reveals defects associated with aging and Hutchinson-Gilford progeria syndrome. <i>eLife</i>. 2020;9. doi:<a href=\"https://doi.org/10.7554/elife.54383\">10.7554/elife.54383</a>","short":"S. Bersini, R. Schulte, L. Huang, H. Tsai, M. Hetzer, ELife 9 (2020).","ieee":"S. Bersini, R. Schulte, L. Huang, H. Tsai, and M. Hetzer, “Direct reprogramming of human smooth muscle and vascular endothelial cells reveals defects associated with aging and Hutchinson-Gilford progeria syndrome,” <i>eLife</i>, vol. 9. eLife Sciences Publications, 2020.","chicago":"Bersini, Simone, Roberta Schulte, Ling Huang, Hannah Tsai, and Martin Hetzer. “Direct Reprogramming of Human Smooth Muscle and Vascular Endothelial Cells Reveals Defects Associated with Aging and Hutchinson-Gilford Progeria Syndrome.” <i>ELife</i>. eLife Sciences Publications, 2020. <a href=\"https://doi.org/10.7554/elife.54383\">https://doi.org/10.7554/elife.54383</a>.","apa":"Bersini, S., Schulte, R., Huang, L., Tsai, H., &#38; Hetzer, M. (2020). Direct reprogramming of human smooth muscle and vascular endothelial cells reveals defects associated with aging and Hutchinson-Gilford progeria syndrome. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.54383\">https://doi.org/10.7554/elife.54383</a>","ista":"Bersini S, Schulte R, Huang L, Tsai H, Hetzer M. 2020. Direct reprogramming of human smooth muscle and vascular endothelial cells reveals defects associated with aging and Hutchinson-Gilford progeria syndrome. eLife. 9, e54383.","mla":"Bersini, Simone, et al. “Direct Reprogramming of Human Smooth Muscle and Vascular Endothelial Cells Reveals Defects Associated with Aging and Hutchinson-Gilford Progeria Syndrome.” <i>ELife</i>, vol. 9, e54383, eLife Sciences Publications, 2020, doi:<a href=\"https://doi.org/10.7554/elife.54383\">10.7554/elife.54383</a>."},"file_date_updated":"2022-04-08T06:53:10Z","article_number":"e54383","scopus_import":"1","language":[{"iso":"eng"}],"type":"journal_article","ddc":["570"],"day":"08","date_published":"2020-09-08T00:00:00Z","date_created":"2022-04-07T07:43:48Z","status":"public","publisher":"eLife Sciences Publications","publication_status":"published","oa_version":"Published Version","title":"Direct reprogramming of human smooth muscle and vascular endothelial cells reveals defects associated with aging and Hutchinson-Gilford progeria syndrome","article_processing_charge":"No","pmid":1,"year":"2020","author":[{"last_name":"Bersini","full_name":"Bersini, Simone","first_name":"Simone"},{"full_name":"Schulte, Roberta","first_name":"Roberta","last_name":"Schulte"},{"last_name":"Huang","first_name":"Ling","full_name":"Huang, Ling"},{"full_name":"Tsai, Hannah","first_name":"Hannah","last_name":"Tsai"},{"full_name":"HETZER, Martin W","first_name":"Martin W","last_name":"HETZER","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","orcid":"0000-0002-2111-992X"}]},{"ddc":["580"],"day":"28","type":"journal_article","language":[{"iso":"eng"}],"scopus_import":"1","date_published":"2019-05-28T00:00:00Z","publication_status":"published","publisher":"eLife Sciences Publications","acknowledgement":"We thank David Twell for the pDONR-P4-P1R-pLAT52 and pDONR-P2R-P3-mRFP vectors, the John Innes Centre Bioimaging Facility (Elaine Barclay and Grant Calder) for their assistance with microscopy, and the Norwich BioScience Institute Partnership Computing infrastructure for Science Group for High Performance Computing resources. This work was funded by a Biotechnology and Biological Sciences Research Council (BBSRC) David Phillips Fellowship (BB/L025043/1; SH, JZ and XF), a European Research Council Starting Grant ('SexMeth' 804981; XF) and a Grant to Exceptional Researchers by the Gatsby Charitable Foundation (SH and XF).","date_created":"2023-01-16T09:17:21Z","status":"public","author":[{"last_name":"He","full_name":"He, Shengbo","first_name":"Shengbo"},{"last_name":"Vickers","first_name":"Martin","full_name":"Vickers, Martin"},{"last_name":"Zhang","full_name":"Zhang, Jingyi","first_name":"Jingyi"},{"id":"e0164712-22ee-11ed-b12a-d80fcdf35958","last_name":"Feng","full_name":"Feng, Xiaoqi","first_name":"Xiaoqi","orcid":"0000-0002-4008-1234"}],"year":"2019","title":"Natural depletion of histone H1 in sex cells causes DNA demethylation, heterochromatin decondensation and transposon activation","article_processing_charge":"No","oa_version":"Published Version","file":[{"creator":"alisjak","checksum":"ea6b89c20d59e5eb3646916fe5d568ad","file_id":"12525","content_type":"application/pdf","file_size":2493837,"date_created":"2023-02-07T09:42:46Z","success":1,"relation":"main_file","access_level":"open_access","date_updated":"2023-02-07T09:42:46Z","file_name":"2019_elife_He.pdf"}],"_id":"12192","abstract":[{"lang":"eng","text":"Transposable elements (TEs), the movement of which can damage the genome, are epigenetically silenced in eukaryotes. Intriguingly, TEs are activated in the sperm companion cell – vegetative cell (VC) – of the flowering plant Arabidopsis thaliana. However, the extent and mechanism of this activation are unknown. Here we show that about 100 heterochromatic TEs are activated in VCs, mostly by DEMETER-catalyzed DNA demethylation. We further demonstrate that DEMETER access to some of these TEs is permitted by the natural depletion of linker histone H1 in VCs. Ectopically expressed H1 suppresses TEs in VCs by reducing DNA demethylation and via a methylation-independent mechanism. We demonstrate that H1 is required for heterochromatin condensation in plant cells and show that H1 overexpression creates heterochromatic foci in the VC progenitor cell. Taken together, our results demonstrate that the natural depletion of H1 during male gametogenesis facilitates DEMETER-directed DNA demethylation, heterochromatin relaxation, and TE activation."}],"intvolume":"         8","article_type":"original","month":"05","volume":8,"keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"publication":"eLife","department":[{"_id":"XiFe"}],"date_updated":"2025-01-14T14:31:41Z","external_id":{"unknown":["31135340"]},"extern":"1","oa":1,"has_accepted_license":"1","doi":"10.7554/elife.42530","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"publication_identifier":{"issn":["2050-084X"]},"article_number":"42530","file_date_updated":"2023-02-07T09:42:46Z","citation":{"short":"S. He, M. Vickers, J. Zhang, X. Feng, ELife 8 (2019).","ama":"He S, Vickers M, Zhang J, Feng X. Natural depletion of histone H1 in sex cells causes DNA demethylation, heterochromatin decondensation and transposon activation. <i>eLife</i>. 2019;8. doi:<a href=\"https://doi.org/10.7554/elife.42530\">10.7554/elife.42530</a>","apa":"He, S., Vickers, M., Zhang, J., &#38; Feng, X. (2019). Natural depletion of histone H1 in sex cells causes DNA demethylation, heterochromatin decondensation and transposon activation. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.42530\">https://doi.org/10.7554/elife.42530</a>","ista":"He S, Vickers M, Zhang J, Feng X. 2019. Natural depletion of histone H1 in sex cells causes DNA demethylation, heterochromatin decondensation and transposon activation. eLife. 8, 42530.","mla":"He, Shengbo, et al. “Natural Depletion of Histone H1 in Sex Cells Causes DNA Demethylation, Heterochromatin Decondensation and Transposon Activation.” <i>ELife</i>, vol. 8, 42530, eLife Sciences Publications, 2019, doi:<a href=\"https://doi.org/10.7554/elife.42530\">10.7554/elife.42530</a>.","chicago":"He, Shengbo, Martin Vickers, Jingyi Zhang, and Xiaoqi Feng. “Natural Depletion of Histone H1 in Sex Cells Causes DNA Demethylation, Heterochromatin Decondensation and Transposon Activation.” <i>ELife</i>. eLife Sciences Publications, 2019. <a href=\"https://doi.org/10.7554/elife.42530\">https://doi.org/10.7554/elife.42530</a>.","ieee":"S. He, M. Vickers, J. Zhang, and X. Feng, “Natural depletion of histone H1 in sex cells causes DNA demethylation, heterochromatin decondensation and transposon activation,” <i>eLife</i>, vol. 8. eLife Sciences Publications, 2019."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","quality_controlled":"1"},{"related_material":{"record":[{"id":"13079","relation":"research_data","status":"public"}]},"date_updated":"2024-10-14T12:08:36Z","external_id":{"pmid":["31599721"]},"oa":1,"extern":"1","article_type":"original","month":"10","file":[{"file_name":"2019_eLife_Buchwalter.pdf","date_updated":"2022-04-08T08:18:01Z","access_level":"open_access","relation":"main_file","content_type":"application/pdf","file_size":6984654,"date_created":"2022-04-08T08:18:01Z","success":1,"file_id":"11138","checksum":"1e8672a1e9c3dc0a2d3d0dad89673616","creator":"dernst"}],"abstract":[{"lang":"eng","text":"The inner nuclear membrane (INM) is a subdomain of the endoplasmic reticulum (ER) that is gated by the nuclear pore complex. It is unknown whether proteins of the INM and ER are degraded through shared or distinct pathways in mammalian cells. We applied dynamic proteomics to profile protein half-lives and report that INM and ER residents turn over at similar rates, indicating that the INM’s unique topology is not a barrier to turnover. Using a microscopy approach, we observed that the proteasome can degrade INM proteins in situ. However, we also uncovered evidence for selective, vesicular transport-mediated turnover of a single INM protein, emerin, that is potentiated by ER stress. Emerin is rapidly cleared from the INM by a mechanism that requires emerin’s LEM domain to mediate vesicular trafficking to lysosomes. This work demonstrates that the INM can be dynamically remodeled in response to environmental inputs."}],"_id":"11060","intvolume":"         8","publication":"eLife","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"volume":8,"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_number":"e49796","file_date_updated":"2022-04-08T08:18:01Z","citation":{"ama":"Buchwalter A, Schulte R, Tsai H, Capitanio J, Hetzer M. Selective clearance of the inner nuclear membrane protein emerin by vesicular transport during ER stress. <i>eLife</i>. 2019;8. doi:<a href=\"https://doi.org/10.7554/elife.49796\">10.7554/elife.49796</a>","short":"A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, M. Hetzer, ELife 8 (2019).","ieee":"A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, and M. Hetzer, “Selective clearance of the inner nuclear membrane protein emerin by vesicular transport during ER stress,” <i>eLife</i>, vol. 8. eLife Sciences Publications, 2019.","chicago":"Buchwalter, Abigail, Roberta Schulte, Hsiao Tsai, Juliana Capitanio, and Martin Hetzer. “Selective Clearance of the Inner Nuclear Membrane Protein Emerin by Vesicular Transport during ER Stress.” <i>ELife</i>. eLife Sciences Publications, 2019. <a href=\"https://doi.org/10.7554/elife.49796\">https://doi.org/10.7554/elife.49796</a>.","mla":"Buchwalter, Abigail, et al. “Selective Clearance of the Inner Nuclear Membrane Protein Emerin by Vesicular Transport during ER Stress.” <i>ELife</i>, vol. 8, e49796, eLife Sciences Publications, 2019, doi:<a href=\"https://doi.org/10.7554/elife.49796\">10.7554/elife.49796</a>.","ista":"Buchwalter A, Schulte R, Tsai H, Capitanio J, Hetzer M. 2019. Selective clearance of the inner nuclear membrane protein emerin by vesicular transport during ER stress. eLife. 8, e49796.","apa":"Buchwalter, A., Schulte, R., Tsai, H., Capitanio, J., &#38; Hetzer, M. (2019). Selective clearance of the inner nuclear membrane protein emerin by vesicular transport during ER stress. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.49796\">https://doi.org/10.7554/elife.49796</a>"},"quality_controlled":"1","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"has_accepted_license":"1","doi":"10.7554/elife.49796","publication_identifier":{"issn":["2050-084X"]},"date_published":"2019-10-10T00:00:00Z","day":"10","ddc":["570"],"type":"journal_article","scopus_import":"1","language":[{"iso":"eng"}],"author":[{"last_name":"Buchwalter","full_name":"Buchwalter, Abigail","first_name":"Abigail"},{"last_name":"Schulte","first_name":"Roberta","full_name":"Schulte, Roberta"},{"first_name":"Hsiao","full_name":"Tsai, Hsiao","last_name":"Tsai"},{"last_name":"Capitanio","first_name":"Juliana","full_name":"Capitanio, Juliana"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","last_name":"HETZER","first_name":"Martin W","full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X"}],"year":"2019","article_processing_charge":"No","title":"Selective clearance of the inner nuclear membrane protein emerin by vesicular transport during ER stress","oa_version":"Published Version","pmid":1,"publisher":"eLife Sciences Publications","publication_status":"published","date_created":"2022-04-07T07:45:02Z","status":"public"},{"type":"journal_article","day":"01","language":[{"iso":"eng"}],"scopus_import":"1","date_published":"2017-08-01T00:00:00Z","publication_status":"published","publisher":"eLife Sciences Publications","date_created":"2024-03-21T07:55:36Z","status":"public","year":"2017","author":[{"full_name":"Fong, Jiunn CN","first_name":"Jiunn CN","last_name":"Fong"},{"first_name":"Andrew","full_name":"Rogers, Andrew","last_name":"Rogers"},{"first_name":"Alicia Kathleen","full_name":"Michael, Alicia Kathleen","last_name":"Michael","id":"6437c950-2a03-11ee-914d-d6476dd7b75c"},{"first_name":"Nicole C","full_name":"Parsley, Nicole C","last_name":"Parsley"},{"last_name":"Cornell","full_name":"Cornell, William-Cole","first_name":"William-Cole"},{"full_name":"Lin, Yu-Cheng","first_name":"Yu-Cheng","last_name":"Lin"},{"last_name":"Singh","first_name":"Praveen K","full_name":"Singh, Praveen K"},{"first_name":"Raimo","full_name":"Hartmann, Raimo","last_name":"Hartmann"},{"full_name":"Drescher, Knut","first_name":"Knut","last_name":"Drescher"},{"last_name":"Vinogradov","full_name":"Vinogradov, Evgeny","first_name":"Evgeny"},{"last_name":"Dietrich","first_name":"Lars EP","full_name":"Dietrich, Lars EP"},{"full_name":"Partch, Carrie L","first_name":"Carrie L","last_name":"Partch"},{"last_name":"Yildiz","full_name":"Yildiz, Fitnat H","first_name":"Fitnat H"}],"pmid":1,"oa_version":"Published Version","article_processing_charge":"Yes","title":"Structural dynamics of RbmA governs plasticity of Vibrio cholerae biofilms","abstract":[{"lang":"eng","text":"Biofilm formation is critical for the infection cycle of Vibrio cholerae. Vibrio exopolysaccharides (VPS) and the matrix proteins RbmA, Bap1 and RbmC are required for the development of biofilm architecture. We demonstrate that RbmA binds VPS directly and uses a binary structural switch within its first fibronectin type III (FnIII-1) domain to control RbmA structural dynamics and the formation of VPS-dependent higher-order structures. The structural switch in FnIII-1 regulates interactions in trans with the FnIII-2 domain, leading to open (monomeric) or closed (dimeric) interfaces. The ability of RbmA to switch between open and closed states is important for V. cholerae biofilm formation, as RbmA variants with switches that are locked in either of the two states lead to biofilms with altered architecture and structural integrity."}],"_id":"15154","intvolume":"         6","article_type":"original","month":"08","volume":6,"keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"publication":"eLife","external_id":{"pmid":["28762945"]},"date_updated":"2024-03-25T12:22:54Z","extern":"1","oa":1,"doi":"10.7554/elife.26163","publication_identifier":{"issn":["2050-084X"]},"citation":{"short":"J.C. Fong, A. Rogers, A.K. Michael, N.C. Parsley, W.-C. Cornell, Y.-C. Lin, P.K. Singh, R. Hartmann, K. Drescher, E. Vinogradov, L.E. Dietrich, C.L. Partch, F.H. Yildiz, ELife 6 (2017).","ama":"Fong JC, Rogers A, Michael AK, et al. Structural dynamics of RbmA governs plasticity of Vibrio cholerae biofilms. <i>eLife</i>. 2017;6. doi:<a href=\"https://doi.org/10.7554/elife.26163\">10.7554/elife.26163</a>","apa":"Fong, J. C., Rogers, A., Michael, A. K., Parsley, N. C., Cornell, W.-C., Lin, Y.-C., … Yildiz, F. H. (2017). Structural dynamics of RbmA governs plasticity of Vibrio cholerae biofilms. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.26163\">https://doi.org/10.7554/elife.26163</a>","ista":"Fong JC, Rogers A, Michael AK, Parsley NC, Cornell W-C, Lin Y-C, Singh PK, Hartmann R, Drescher K, Vinogradov E, Dietrich LE, Partch CL, Yildiz FH. 2017. Structural dynamics of RbmA governs plasticity of Vibrio cholerae biofilms. eLife. 6, 26163.","mla":"Fong, Jiunn CN, et al. “Structural Dynamics of RbmA Governs Plasticity of Vibrio Cholerae Biofilms.” <i>ELife</i>, vol. 6, 26163, eLife Sciences Publications, 2017, doi:<a href=\"https://doi.org/10.7554/elife.26163\">10.7554/elife.26163</a>.","chicago":"Fong, Jiunn CN, Andrew Rogers, Alicia K. Michael, Nicole C Parsley, William-Cole Cornell, Yu-Cheng Lin, Praveen K Singh, et al. “Structural Dynamics of RbmA Governs Plasticity of Vibrio Cholerae Biofilms.” <i>ELife</i>. eLife Sciences Publications, 2017. <a href=\"https://doi.org/10.7554/elife.26163\">https://doi.org/10.7554/elife.26163</a>.","ieee":"J. C. Fong <i>et al.</i>, “Structural dynamics of RbmA governs plasticity of Vibrio cholerae biofilms,” <i>eLife</i>, vol. 6. eLife Sciences Publications, 2017."},"article_number":"26163","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","main_file_link":[{"open_access":"1","url":"https://doi.org/10.7554/eLife.26163"}],"quality_controlled":"1"},{"quality_controlled":"1","article_number":"e30292","file_date_updated":"2021-11-29T09:07:41Z","citation":{"mla":"Helle, Sebastian Carsten Johannes, et al. “Mechanical Force Induces Mitochondrial Fission.” <i>ELife</i>, vol. 6, e30292, eLife Sciences Publications, 2017, doi:<a href=\"https://doi.org/10.7554/elife.30292\">10.7554/elife.30292</a>.","ista":"Helle SCJ, Feng Q, Aebersold MJ, Hirt L, Grüter RR, Vahid A, Sirianni A, Mostowy S, Snedeker JG, Šarić A, Idema T, Zambelli T, Kornmann B. 2017. Mechanical force induces mitochondrial fission. eLife. 6, e30292.","apa":"Helle, S. C. J., Feng, Q., Aebersold, M. J., Hirt, L., Grüter, R. R., Vahid, A., … Kornmann, B. (2017). Mechanical force induces mitochondrial fission. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.30292\">https://doi.org/10.7554/elife.30292</a>","chicago":"Helle, Sebastian Carsten Johannes, Qian Feng, Mathias J Aebersold, Luca Hirt, Raphael R Grüter, Afshin Vahid, Andrea Sirianni, et al. “Mechanical Force Induces Mitochondrial Fission.” <i>ELife</i>. eLife Sciences Publications, 2017. <a href=\"https://doi.org/10.7554/elife.30292\">https://doi.org/10.7554/elife.30292</a>.","ieee":"S. C. J. Helle <i>et al.</i>, “Mechanical force induces mitochondrial fission,” <i>eLife</i>, vol. 6. eLife Sciences Publications, 2017.","short":"S.C.J. Helle, Q. Feng, M.J. Aebersold, L. Hirt, R.R. Grüter, A. Vahid, A. Sirianni, S. Mostowy, J.G. Snedeker, A. Šarić, T. Idema, T. Zambelli, B. Kornmann, ELife 6 (2017).","ama":"Helle SCJ, Feng Q, Aebersold MJ, et al. Mechanical force induces mitochondrial fission. <i>eLife</i>. 2017;6. doi:<a href=\"https://doi.org/10.7554/elife.30292\">10.7554/elife.30292</a>"},"main_file_link":[{"open_access":"1","url":"https://elifesciences.org/articles/30292"}],"user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","publication_identifier":{"issn":["2050-084X"]},"has_accepted_license":"1","doi":"10.7554/elife.30292","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)"},"extern":"1","oa":1,"date_updated":"2021-11-29T09:28:14Z","external_id":{"pmid":["29119945"]},"volume":6,"keyword":["general immunology and microbiology","general biochemistry","genetics and molecular biology","general medicine","general neuroscience"],"publication":"eLife","file":[{"success":1,"date_created":"2021-11-29T09:07:41Z","file_size":6120157,"content_type":"application/pdf","file_id":"10372","checksum":"c35f42dcfb007f6d6c761a27e24c26d3","creator":"cchlebak","file_name":"2017_eLife_Helle.pdf","access_level":"open_access","date_updated":"2021-11-29T09:07:41Z","relation":"main_file"}],"intvolume":"         6","_id":"10370","abstract":[{"lang":"eng","text":"Eukaryotic cells are densely packed with macromolecular complexes and intertwining organelles, continually transported and reshaped. Intriguingly, organelles avoid clashing and entangling with each other in such limited space. Mitochondria form extensive networks constantly remodeled by fission and fusion. Here, we show that mitochondrial fission is triggered by mechanical forces. Mechano-stimulation of mitochondria – via encounter with motile intracellular pathogens, via external pressure applied by an atomic force microscope, or via cell migration across uneven microsurfaces – results in the recruitment of the mitochondrial fission machinery, and subsequent division. We propose that MFF, owing to affinity for narrow mitochondria, acts as a membrane-bound force sensor to recruit the fission machinery to mechanically strained sites. Thus, mitochondria adapt to the environment by sensing and responding to biomechanical cues. Our findings that mechanical triggers can be coupled to biochemical responses in membrane dynamics may explain how organelles orderly cohabit in the crowded cytoplasm."}],"article_type":"original","month":"11","pmid":1,"article_processing_charge":"No","title":"Mechanical force induces mitochondrial fission","oa_version":"Published Version","author":[{"last_name":"Helle","full_name":"Helle, Sebastian Carsten Johannes","first_name":"Sebastian Carsten Johannes"},{"last_name":"Feng","full_name":"Feng, Qian","first_name":"Qian"},{"full_name":"Aebersold, Mathias J","first_name":"Mathias J","last_name":"Aebersold"},{"last_name":"Hirt","full_name":"Hirt, Luca","first_name":"Luca"},{"full_name":"Grüter, Raphael R","first_name":"Raphael R","last_name":"Grüter"},{"last_name":"Vahid","first_name":"Afshin","full_name":"Vahid, Afshin"},{"last_name":"Sirianni","full_name":"Sirianni, Andrea","first_name":"Andrea"},{"full_name":"Mostowy, Serge","first_name":"Serge","last_name":"Mostowy"},{"last_name":"Snedeker","full_name":"Snedeker, Jess G","first_name":"Jess G"},{"last_name":"Šarić","id":"bf63d406-f056-11eb-b41d-f263a6566d8b","first_name":"Anđela","full_name":"Šarić, Anđela","orcid":"0000-0002-7854-2139"},{"last_name":"Idema","first_name":"Timon","full_name":"Idema, Timon"},{"last_name":"Zambelli","full_name":"Zambelli, Tomaso","first_name":"Tomaso"},{"last_name":"Kornmann","full_name":"Kornmann, Benoît","first_name":"Benoît"}],"year":"2017","date_created":"2021-11-29T08:51:38Z","status":"public","publication_status":"published","publisher":"eLife Sciences Publications","date_published":"2017-11-09T00:00:00Z","language":[{"iso":"eng"}],"scopus_import":"1","ddc":["572"],"day":"09","type":"journal_article"}]