[{"project":[{"call_identifier":"H2020","_id":"261099A6-B435-11E9-9278-68D0E5697425","name":"Tracing Evolution of Auxin Transport and Polarity in Plants","grant_number":"742985"},{"_id":"26538374-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Molecular mechanisms of endocytic cargo recognition in plants","grant_number":"I03630"}],"citation":{"mla":"Adamowski, Maciek, et al. “Developmental Patterning Function of GNOM ARF-GEF Mediated from the Cell Periphery.” ELife, vol. 13, eLife Sciences Publications, 2024, doi:10.7554/elife.68993.","ama":"Adamowski M, Matijevic I, Friml J. Developmental patterning function of GNOM ARF-GEF mediated from the cell periphery. eLife. 2024;13. doi:10.7554/elife.68993","apa":"Adamowski, M., Matijevic, I., & Friml, J. (2024). Developmental patterning function of GNOM ARF-GEF mediated from the cell periphery. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.68993","ieee":"M. Adamowski, I. Matijevic, and J. Friml, “Developmental patterning function of GNOM ARF-GEF mediated from the cell periphery,” eLife, vol. 13. eLife Sciences Publications, 2024.","short":"M. Adamowski, I. Matijevic, J. Friml, ELife 13 (2024).","chicago":"Adamowski, Maciek, Ivana Matijevic, and Jiří Friml. “Developmental Patterning Function of GNOM ARF-GEF Mediated from the Cell Periphery.” ELife. eLife Sciences Publications, 2024. https://doi.org/10.7554/elife.68993.","ista":"Adamowski M, Matijevic I, Friml J. 2024. Developmental patterning function of GNOM ARF-GEF mediated from the cell periphery. eLife. 13."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"Yes","author":[{"last_name":"Adamowski","full_name":"Adamowski, Maciek","orcid":"0000-0001-6463-5257","first_name":"Maciek","id":"45F536D2-F248-11E8-B48F-1D18A9856A87"},{"id":"83c17ce3-15b2-11ec-abd3-f486545870bd","first_name":"Ivana","last_name":"Matijevic","full_name":"Matijevic, Ivana"},{"last_name":"Friml","full_name":"Friml, Jiří","orcid":"0000-0002-8302-7596","id":"4159519E-F248-11E8-B48F-1D18A9856A87","first_name":"Jiří"}],"title":"Developmental patterning function of GNOM ARF-GEF mediated from the cell periphery","acknowledgement":"The authors would like to gratefully acknowledge Dr Xixi Zhang for cloning the GNL1/pDONR221 construct and for useful discussions.H2020 European Research\r\nCouncil Advanced Grant ETAP742985 to Jiří Friml, Austrian Science Fund I 3630-B25 to Jiří Friml","oa":1,"quality_controlled":"1","publisher":"eLife Sciences Publications","year":"2024","has_accepted_license":"1","publication":"eLife","day":"21","date_created":"2024-02-27T07:10:11Z","doi":"10.7554/elife.68993","date_published":"2024-02-21T00:00:00Z","_id":"15033","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"original","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"status":"public","date_updated":"2024-02-28T12:29:43Z","ddc":["580"],"department":[{"_id":"JiFr"}],"abstract":[{"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 gn knockouts. The functional GN mutant variant GNfewerroots, 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.","lang":"eng"}],"oa_version":"Published Version","main_file_link":[{"url":"https://doi.org/10.7554/eLife.68993","open_access":"1"}],"intvolume":" 13","month":"02","publication_status":"epub_ahead","publication_identifier":{"issn":["2050-084X"]},"language":[{"iso":"eng"}],"ec_funded":1,"volume":13},{"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"article_type":"review","type":"journal_article","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Neuroscience"],"status":"public","_id":"14683","department":[{"_id":"SiHi"}],"date_updated":"2023-12-18T08:06:14Z","ddc":["570"],"main_file_link":[{"url":"https://doi.org/10.1016/j.xpro.2023.102771","open_access":"1"}],"scopus_import":"1","intvolume":" 5","month":"12","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"}],"acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"oa_version":"Submitted Version","pmid":1,"ec_funded":1,"issue":"1","volume":5,"publication_status":"epub_ahead","publication_identifier":{"issn":["2666-1667"]},"language":[{"iso":"eng"}],"project":[{"call_identifier":"FWF","_id":"268F8446-B435-11E9-9278-68D0E5697425","name":"Role of Eed in neural stem cell lineage progression","grant_number":"T0101031"},{"name":"ISTplus - Postdoctoral Fellowships","grant_number":"754411","call_identifier":"H2020","_id":"260C2330-B435-11E9-9278-68D0E5697425"},{"_id":"059F6AB4-7A3F-11EA-A408-12923DDC885E","grant_number":"F07805","name":"Molecular Mechanisms of Neural Stem Cell Lineage Progression"},{"_id":"260018B0-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"725780","name":"Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development"}],"article_number":"102771","article_processing_charge":"No","external_id":{"pmid":["38070137"]},"author":[{"id":"4CD6AAC6-F248-11E8-B48F-1D18A9856A87","first_name":"Nicole","last_name":"Amberg","full_name":"Amberg, Nicole","orcid":"0000-0002-3183-8207"},{"full_name":"Cheung, Giselle T","orcid":"0000-0001-8457-2572","last_name":"Cheung","first_name":"Giselle T","id":"471195F6-F248-11E8-B48F-1D18A9856A87"},{"id":"37B36620-F248-11E8-B48F-1D18A9856A87","first_name":"Simon","full_name":"Hippenmeyer, Simon","orcid":"0000-0003-2279-1061","last_name":"Hippenmeyer"}],"title":"Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry","citation":{"ista":"Amberg N, Cheung GT, Hippenmeyer S. 2023. Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols. 5(1), 102771.","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.” STAR Protocols. Elsevier, 2023. https://doi.org/10.1016/j.xpro.2023.102771.","apa":"Amberg, N., Cheung, G. T., & Hippenmeyer, S. (2023). Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols. Elsevier. https://doi.org/10.1016/j.xpro.2023.102771","ama":"Amberg N, Cheung GT, Hippenmeyer S. Protocol for sorting cells from mouse brains labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols. 2023;5(1). doi:10.1016/j.xpro.2023.102771","short":"N. Amberg, G.T. Cheung, S. Hippenmeyer, STAR Protocols 5 (2023).","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,” STAR Protocols, vol. 5, no. 1. Elsevier, 2023.","mla":"Amberg, Nicole, et al. “Protocol for Sorting Cells from Mouse Brains Labeled with Mosaic Analysis with Double Markers by Flow Cytometry.” STAR Protocols, vol. 5, no. 1, 102771, Elsevier, 2023, doi:10.1016/j.xpro.2023.102771."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","oa":1,"publisher":"Elsevier","quality_controlled":"1","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","date_published":"2023-12-08T00:00:00Z","doi":"10.1016/j.xpro.2023.102771","year":"2023","publication":"STAR Protocols","day":"08"},{"external_id":{"pmid":["35019710"],"isi":["000779305000033"]},"article_processing_charge":"No","author":[{"first_name":"Stefan","full_name":"Windhaber, Stefan","last_name":"Windhaber"},{"last_name":"Xin","full_name":"Xin, Qilin","first_name":"Qilin"},{"first_name":"Zina M.","last_name":"Uckeley","full_name":"Uckeley, Zina M."},{"last_name":"Koch","full_name":"Koch, Jana","first_name":"Jana"},{"first_name":"Martin","id":"4741CA5A-F248-11E8-B48F-1D18A9856A87","full_name":"Obr, Martin","last_name":"Obr"},{"first_name":"Céline","last_name":"Garnier","full_name":"Garnier, Céline"},{"first_name":"Catherine","last_name":"Luengo-Guyonnot","full_name":"Luengo-Guyonnot, Catherine"},{"last_name":"Duboeuf","full_name":"Duboeuf, Maëva","first_name":"Maëva"},{"last_name":"Schur","orcid":"0000-0003-4790-8078","full_name":"Schur, Florian KM","first_name":"Florian KM","id":"48AD8942-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Pierre-Yves","full_name":"Lozach, Pierre-Yves","last_name":"Lozach"}],"title":"The Orthobunyavirus Germiston enters host cells from late endosomes","citation":{"ista":"Windhaber S, Xin Q, Uckeley ZM, Koch J, Obr M, Garnier C, Luengo-Guyonnot C, Duboeuf M, Schur FK, Lozach P-Y. 2022. The Orthobunyavirus Germiston enters host cells from late endosomes. Journal of Virology. 96(5), e02146-21.","chicago":"Windhaber, Stefan, Qilin Xin, Zina M. Uckeley, Jana Koch, Martin Obr, Céline Garnier, Catherine Luengo-Guyonnot, Maëva Duboeuf, Florian KM Schur, and Pierre-Yves Lozach. “The Orthobunyavirus Germiston Enters Host Cells from Late Endosomes.” Journal of Virology. American Society for Microbiology, 2022. https://doi.org/10.1128/jvi.02146-21.","short":"S. Windhaber, Q. Xin, Z.M. Uckeley, J. Koch, M. Obr, C. Garnier, C. Luengo-Guyonnot, M. Duboeuf, F.K. Schur, P.-Y. Lozach, Journal of Virology 96 (2022).","ieee":"S. Windhaber et al., “The Orthobunyavirus Germiston enters host cells from late endosomes,” Journal of Virology, vol. 96, no. 5. American Society for Microbiology, 2022.","apa":"Windhaber, S., Xin, Q., Uckeley, Z. M., Koch, J., Obr, M., Garnier, C., … Lozach, P.-Y. (2022). The Orthobunyavirus Germiston enters host cells from late endosomes. Journal of Virology. American Society for Microbiology. https://doi.org/10.1128/jvi.02146-21","ama":"Windhaber S, Xin Q, Uckeley ZM, et al. The Orthobunyavirus Germiston enters host cells from late endosomes. Journal of Virology. 2022;96(5). doi:10.1128/jvi.02146-21","mla":"Windhaber, Stefan, et al. “The Orthobunyavirus Germiston Enters Host Cells from Late Endosomes.” Journal of Virology, vol. 96, no. 5, e02146-21, American Society for Microbiology, 2022, doi:10.1128/jvi.02146-21."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","project":[{"grant_number":"P31445","name":"Structural conservation and diversity in retroviral capsid","_id":"26736D6A-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"article_number":"e02146-21","date_created":"2022-01-18T10:04:18Z","date_published":"2022-03-01T00:00:00Z","doi":"10.1128/jvi.02146-21","year":"2022","isi":1,"publication":"Journal of Virology","day":"01","oa":1,"quality_controlled":"1","publisher":"American Society for Microbiology","acknowledgement":"This work was supported by INRAE starter funds, Project IDEXLYON (University of Lyon) within the Programme Investissements d’Avenir (ANR-16-IDEX-0005), and FINOVIAO14 (Fondation pour l’Université de Lyon), all to P.Y.L. This work was also supported by CellNetworks Research Group funds and Deutsche Forschungsgemeinschaft (DFG) funding (grant numbers LO-2338/1-1 and LO-2338/3-1) awarded to P.Y.L., Austrian Science Fund (FWF) grant P31445 to F.K.M.S., a Chinese Scholarship Council (CSC;no. 201904910701) fellowship to Q.X., and a ministére de l’enseignement supérieur, de la recherche et de l’innovation (MESRI) doctoral thesis grant to M.D.","department":[{"_id":"FlSc"}],"date_updated":"2023-08-02T13:52:33Z","article_type":"original","type":"journal_article","keyword":["virology","insect science","immunology","microbiology"],"status":"public","_id":"10639","volume":96,"issue":"5","publication_status":"published","publication_identifier":{"issn":["0022-538X"],"eissn":["1098-5514"]},"language":[{"iso":"eng"}],"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8906410"}],"scopus_import":"1","intvolume":" 96","month":"03","acknowledged_ssus":[{"_id":"EM-Fac"}],"abstract":[{"text":"With more than 80 members worldwide, the Orthobunyavirus genus in the Peribunyaviridae family is a large genus of enveloped RNA viruses, many of which are emerging pathogens in humans and livestock. How orthobunyaviruses (OBVs) penetrate and infect mammalian host cells remains poorly characterized. Here, we investigated the entry mechanisms of the OBV Germiston (GERV). Viral particles were visualized by cryo-electron microscopy and appeared roughly spherical with an average diameter of 98 nm. Labeling of the virus with fluorescent dyes did not adversely affect its infectivity and allowed the monitoring of single particles in fixed and live cells. Using this approach, we found that endocytic internalization of bound viruses was asynchronous and occurred within 30-40 min. The virus entered Rab5a+ early endosomes and, subsequently, late endosomal vacuoles containing Rab7a but not LAMP-1. Infectious entry did not require proteolytic cleavage, and endosomal acidification was sufficient and necessary for viral fusion. Acid-activated penetration began 15-25 min after initiation of virus internalization and relied on maturation of early endosomes to late endosomes. The optimal pH for viral membrane fusion was slightly below 6.0, and penetration was hampered when the potassium influx was abolished. Overall, our study provides real-time visualization of GERV entry into host cells and demonstrates the importance of late endosomal maturation in facilitating OBV penetration.","lang":"eng"}],"pmid":1,"oa_version":"Published Version"},{"abstract":[{"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.","lang":"eng"}],"pmid":1,"oa_version":"None","scopus_import":"1","month":"08","intvolume":" 20","publication_identifier":{"issn":["1740-1526"],"eissn":["1740-1534"]},"publication_status":"published","language":[{"iso":"eng"}],"volume":20,"_id":"10812","article_type":"review","type":"journal_article","status":"public","keyword":["General Immunology and Microbiology","Microbiology","Infectious Diseases"],"date_updated":"2023-08-02T14:41:44Z","department":[{"_id":"CaGu"}],"acknowledgement":"The authors thank B. Kavčič and H. Schulenburg for constructive feedback on the manuscript.","quality_controlled":"1","publisher":"Springer Nature","isi":1,"year":"2022","day":"01","publication":"Nature Reviews Microbiology","page":"478-490","date_published":"2022-08-01T00:00:00Z","doi":"10.1038/s41579-022-00700-5","date_created":"2022-03-04T04:33:49Z","citation":{"ieee":"R. Römhild, M. T. Bollenbach, and D. I. Andersson, “The physiology and genetics of bacterial responses to antibiotic combinations,” Nature Reviews Microbiology, vol. 20. Springer Nature, pp. 478–490, 2022.","short":"R. Römhild, M.T. Bollenbach, D.I. Andersson, Nature Reviews Microbiology 20 (2022) 478–490.","ama":"Römhild R, Bollenbach MT, Andersson DI. The physiology and genetics of bacterial responses to antibiotic combinations. Nature Reviews Microbiology. 2022;20:478-490. doi:10.1038/s41579-022-00700-5","apa":"Römhild, R., Bollenbach, M. T., & Andersson, D. I. (2022). The physiology and genetics of bacterial responses to antibiotic combinations. Nature Reviews Microbiology. Springer Nature. https://doi.org/10.1038/s41579-022-00700-5","mla":"Römhild, Roderich, et al. “The Physiology and Genetics of Bacterial Responses to Antibiotic Combinations.” Nature Reviews Microbiology, vol. 20, Springer Nature, 2022, pp. 478–90, doi:10.1038/s41579-022-00700-5.","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.” Nature Reviews Microbiology. Springer Nature, 2022. https://doi.org/10.1038/s41579-022-00700-5."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","author":[{"last_name":"Römhild","full_name":"Römhild, Roderich","orcid":"0000-0001-9480-5261","first_name":"Roderich","id":"68E56E44-62B0-11EA-B963-444F3DDC885E"},{"first_name":"Mark Tobias","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","last_name":"Bollenbach","orcid":"0000-0003-4398-476X","full_name":"Bollenbach, Mark Tobias"},{"last_name":"Andersson","full_name":"Andersson, Dan I.","first_name":"Dan I."}],"article_processing_charge":"No","external_id":{"pmid":["35241807"],"isi":["000763891900001"]},"title":"The physiology and genetics of bacterial responses to antibiotic combinations"},{"file":[{"relation":"main_file","access_level":"open_access","content_type":"application/pdf","success":1,"file_id":"11454","checksum":"7573c28f44028ab0cc81faef30039e44","creator":"dernst","file_size":5297213,"date_updated":"2022-06-20T07:44:19Z","file_name":"2022_eLife_Somermeyer.pdf","date_created":"2022-06-20T07:44:19Z"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2050-084X"]},"publication_status":"published","volume":11,"ec_funded":1,"oa_version":"Published Version","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"}],"acknowledged_ssus":[{"_id":"LifeSc"},{"_id":"Bio"}],"month":"05","intvolume":" 11","scopus_import":"1","ddc":["570"],"date_updated":"2023-08-03T07:20:15Z","department":[{"_id":"GradSch"},{"_id":"FyKo"}],"file_date_updated":"2022-06-20T07:44:19Z","_id":"11448","status":"public","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"type":"journal_article","article_type":"original","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"day":"05","publication":"eLife","isi":1,"has_accepted_license":"1","year":"2022","doi":"10.7554/elife.75842","date_published":"2022-05-05T00:00:00Z","date_created":"2022-06-18T09:06:59Z","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","quality_controlled":"1","oa":1,"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"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. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.75842","ama":"Gonzalez Somermeyer L, Fleiss A, Mishin AS, et al. Heterogeneity of the GFP fitness landscape and data-driven protein design. eLife. 2022;11. doi:10.7554/elife.75842","ieee":"L. Gonzalez Somermeyer et al., “Heterogeneity of the GFP fitness landscape and data-driven protein design,” eLife, vol. 11. eLife Sciences Publications, 2022.","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).","mla":"Gonzalez Somermeyer, Louisa, et al. “Heterogeneity of the GFP Fitness Landscape and Data-Driven Protein Design.” ELife, vol. 11, 75842, eLife Sciences Publications, 2022, doi:10.7554/elife.75842.","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.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/elife.75842."},"title":"Heterogeneity of the GFP fitness landscape and data-driven protein design","author":[{"full_name":"Gonzalez Somermeyer, Louisa","orcid":"0000-0001-9139-5383","last_name":"Gonzalez Somermeyer","first_name":"Louisa","id":"4720D23C-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Aubin","last_name":"Fleiss","full_name":"Fleiss, Aubin"},{"first_name":"Alexander S","last_name":"Mishin","full_name":"Mishin, Alexander S"},{"first_name":"Nina G","last_name":"Bozhanova","full_name":"Bozhanova, Nina G"},{"full_name":"Igolkina, Anna A","last_name":"Igolkina","first_name":"Anna A"},{"first_name":"Jens","full_name":"Meiler, Jens","last_name":"Meiler"},{"full_name":"Alaball Pujol, Maria-Elisenda","last_name":"Alaball Pujol","first_name":"Maria-Elisenda"},{"full_name":"Putintseva, Ekaterina V","last_name":"Putintseva","first_name":"Ekaterina V"},{"first_name":"Karen S","full_name":"Sarkisyan, Karen S","last_name":"Sarkisyan"},{"last_name":"Kondrashov","full_name":"Kondrashov, Fyodor","orcid":"0000-0001-8243-4694","first_name":"Fyodor","id":"44FDEF62-F248-11E8-B48F-1D18A9856A87"}],"article_processing_charge":"No","external_id":{"isi":["000799197200001"]},"article_number":"75842","project":[{"_id":"26580278-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","name":"Characterizing the fitness landscape on population and global scales","grant_number":"771209"},{"grant_number":"665385","name":"International IST Doctoral Program","_id":"2564DBCA-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"}]},{"title":"Atypical enteropathogenic E. coli are associated with disease activity in ulcerative colitis","author":[{"last_name":"Baumgartner","full_name":"Baumgartner, Maximilian","first_name":"Maximilian"},{"first_name":"Rebecca","last_name":"Zirnbauer","full_name":"Zirnbauer, Rebecca"},{"full_name":"Schlager, Sabine","last_name":"Schlager","first_name":"Sabine"},{"first_name":"Daniel","full_name":"Mertens, Daniel","last_name":"Mertens"},{"first_name":"Nikolaus","last_name":"Gasche","full_name":"Gasche, Nikolaus"},{"last_name":"Sladek","full_name":"Sladek, Barbara","first_name":"Barbara"},{"full_name":"Herbold, Craig","last_name":"Herbold","first_name":"Craig"},{"full_name":"Bochkareva, Olga","last_name":"Bochkareva","first_name":"Olga"},{"last_name":"Emelianenko","full_name":"Emelianenko, Vera","first_name":"Vera","id":"20152b9d-927a-11ed-8107-be36d740812d"},{"first_name":"Harald","last_name":"Vogelsang","full_name":"Vogelsang, Harald"},{"first_name":"Michaela","last_name":"Lang","full_name":"Lang, Michaela"},{"first_name":"Anton","last_name":"Klotz","full_name":"Klotz, Anton"},{"first_name":"Birgit","full_name":"Moik, Birgit","last_name":"Moik"},{"full_name":"Makristathis, Athanasios","last_name":"Makristathis","first_name":"Athanasios"},{"first_name":"David","full_name":"Berry, David","last_name":"Berry"},{"first_name":"Stefanie","last_name":"Dabsch","full_name":"Dabsch, Stefanie"},{"first_name":"Vineeta","last_name":"Khare","full_name":"Khare, Vineeta"},{"last_name":"Gasche","full_name":"Gasche, Christoph","first_name":"Christoph"}],"external_id":{"isi":["000889180100001"]},"article_processing_charge":"No","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"chicago":"Baumgartner, Maximilian, Rebecca Zirnbauer, Sabine Schlager, Daniel Mertens, Nikolaus Gasche, Barbara Sladek, Craig Herbold, et al. “Atypical Enteropathogenic E. Coli Are Associated with Disease Activity in Ulcerative Colitis.” Gut Microbes. Taylor & Francis, 2022. https://doi.org/10.1080/19490976.2022.2143218.","ista":"Baumgartner M, Zirnbauer R, Schlager S, Mertens D, Gasche N, Sladek B, Herbold C, Bochkareva O, Emelianenko V, Vogelsang H, Lang M, Klotz A, Moik B, Makristathis A, Berry D, Dabsch S, Khare V, Gasche C. 2022. Atypical enteropathogenic E. coli are associated with disease activity in ulcerative colitis. Gut Microbes. 14(1), e2143218.","mla":"Baumgartner, Maximilian, et al. “Atypical Enteropathogenic E. Coli Are Associated with Disease Activity in Ulcerative Colitis.” Gut Microbes, vol. 14, no. 1, e2143218, Taylor & Francis, 2022, doi:10.1080/19490976.2022.2143218.","ieee":"M. Baumgartner et al., “Atypical enteropathogenic E. coli are associated with disease activity in ulcerative colitis,” Gut Microbes, vol. 14, no. 1. Taylor & Francis, 2022.","short":"M. Baumgartner, R. Zirnbauer, S. Schlager, D. Mertens, N. Gasche, B. Sladek, C. Herbold, O. Bochkareva, V. Emelianenko, H. Vogelsang, M. Lang, A. Klotz, B. Moik, A. Makristathis, D. Berry, S. Dabsch, V. Khare, C. Gasche, Gut Microbes 14 (2022).","ama":"Baumgartner M, Zirnbauer R, Schlager S, et al. Atypical enteropathogenic E. coli are associated with disease activity in ulcerative colitis. Gut Microbes. 2022;14(1). doi:10.1080/19490976.2022.2143218","apa":"Baumgartner, M., Zirnbauer, R., Schlager, S., Mertens, D., Gasche, N., Sladek, B., … Gasche, C. (2022). Atypical enteropathogenic E. coli are associated with disease activity in ulcerative colitis. Gut Microbes. Taylor & Francis. https://doi.org/10.1080/19490976.2022.2143218"},"article_number":"e2143218","date_published":"2022-11-22T00:00:00Z","doi":"10.1080/19490976.2022.2143218","date_created":"2023-01-12T12:11:36Z","day":"22","publication":"Gut Microbes","has_accepted_license":"1","isi":1,"year":"2022","quality_controlled":"1","publisher":"Taylor & Francis","oa":1,"acknowledgement":"We would like to acknowledge Anita Krnjic, Christina Gmainer, Marion Nehr, Helga Mock, and Sena Ecin for technical support in conducting the experiments.\r\nThis study was supported by the Austrian Science Fund (P 32302) and the Vienna Science and Technology Fund (LS18- 053; Austrian Science Fund (FWF)) [P 32302].","file_date_updated":"2023-01-26T10:56:51Z","department":[{"_id":"FyKo"}],"ddc":["570"],"date_updated":"2023-08-04T09:10:18Z","status":"public","keyword":["Infectious Diseases","Microbiology (medical)","Gastroenterology","Microbiology"],"article_type":"original","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"_id":"12173","volume":14,"issue":"1","file":[{"file_size":4075251,"date_updated":"2023-01-26T10:56:51Z","creator":"dernst","file_name":"2022_GutMicrobes_Baumgartner.pdf","date_created":"2023-01-26T10:56:51Z","content_type":"application/pdf","relation":"main_file","access_level":"open_access","success":1,"file_id":"12400","checksum":"ee7681a17ae27645e9b5c1df61c15429"}],"language":[{"iso":"eng"}],"publication_identifier":{"eissn":["1949-0984"],"issn":["1949-0976"]},"publication_status":"published","month":"11","intvolume":" 14","scopus_import":"1","oa_version":"Published Version","abstract":[{"lang":"eng","text":"With increasing urbanization and industrialization, the prevalence of inflammatory bowel diseases (IBDs) has steadily been rising over the past two decades. IBD involves flares of gastrointestinal (GI) inflammation accompanied by microbiota perturbations. However, microbial mechanisms that trigger such flares remain elusive. Here, we analyzed the association of the emerging pathogen atypical enteropathogenic E. coli (aEPEC) with IBD disease activity. The presence of diarrheagenic E. coli was assessed in stool samples from 630 IBD patients and 234 age- and sex-matched controls without GI symptoms. Microbiota was analyzed with 16S ribosomal RNA gene amplicon sequencing, and 57 clinical aEPEC isolates were subjected to whole-genome sequencing and in vitro pathogenicity experiments including biofilm formation, epithelial barrier function and the ability to induce pro-inflammatory signaling. The presence of aEPEC correlated with laboratory, clinical and endoscopic disease activity in ulcerative colitis (UC), as well as microbiota dysbiosis. In vitro, aEPEC strains induce epithelial p21-activated kinases, disrupt the epithelial barrier and display potent biofilm formation. The effector proteins espV and espG2 distinguish aEPEC cultured from UC and Crohn’s disease patients, respectively. EspV-positive aEPEC harbor more virulence factors and have a higher pro-inflammatory potential, which is counteracted by 5-ASA. aEPEC may tip a fragile immune–microbiota homeostasis and thereby contribute to flares in UC. aEPEC isolates from UC patients display properties to disrupt the epithelial barrier and to induce pro-inflammatory signaling in vitro."}]},{"publication_status":"published","publication_identifier":{"eissn":["2050-084X"]},"language":[{"iso":"eng"}],"file":[{"content_type":"application/pdf","relation":"main_file","access_level":"open_access","success":1,"checksum":"28de155b231ac1c8d4501c98b2fb359a","file_id":"12363","file_size":18935612,"date_updated":"2023-01-24T12:21:32Z","creator":"dernst","file_name":"2022_eLife_Hayward.pdf","date_created":"2023-01-24T12:21:32Z"}],"volume":11,"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."}],"oa_version":"Published Version","scopus_import":"1","intvolume":" 11","month":"09","date_updated":"2023-08-04T09:04:58Z","ddc":["570"],"department":[{"_id":"NiBa"}],"file_date_updated":"2023-01-24T12:21:32Z","_id":"12157","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"article_type":"original","type":"journal_article","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"status":"public","year":"2022","has_accepted_license":"1","isi":1,"publication":"eLife","day":"26","date_created":"2023-01-12T12:09:00Z","date_published":"2022-09-26T00:00:00Z","doi":"10.7554/elife.66697","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","oa":1,"quality_controlled":"1","publisher":"eLife Sciences Publications","citation":{"short":"L. Hayward, G. Sella, ELife 11 (2022).","ieee":"L. Hayward and G. Sella, “Polygenic adaptation after a sudden change in environment,” eLife, vol. 11. eLife Sciences Publications, 2022.","apa":"Hayward, L., & Sella, G. (2022). Polygenic adaptation after a sudden change in environment. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.66697","ama":"Hayward L, Sella G. Polygenic adaptation after a sudden change in environment. eLife. 2022;11. doi:10.7554/elife.66697","mla":"Hayward, Laura, and Guy Sella. “Polygenic Adaptation after a Sudden Change in Environment.” ELife, vol. 11, 66697, eLife Sciences Publications, 2022, doi:10.7554/elife.66697.","ista":"Hayward L, Sella G. 2022. Polygenic adaptation after a sudden change in environment. eLife. 11, 66697.","chicago":"Hayward, Laura, and Guy Sella. “Polygenic Adaptation after a Sudden Change in Environment.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/elife.66697."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","article_processing_charge":"No","external_id":{"isi":["000890735600001"]},"author":[{"id":"fc885ee5-24bf-11eb-ad7b-bcc5104c0c1b","first_name":"Laura","full_name":"Hayward, Laura","last_name":"Hayward"},{"first_name":"Guy","last_name":"Sella","full_name":"Sella, Guy"}],"title":"Polygenic adaptation after a sudden change in environment","article_number":"66697"},{"scopus_import":"1","intvolume":" 18","month":"09","abstract":[{"lang":"eng","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."}],"acknowledged_ssus":[{"_id":"M-Shop"}],"oa_version":"Published Version","issue":"9","volume":18,"publication_status":"published","publication_identifier":{"eissn":["1744-4292"]},"language":[{"iso":"eng"}],"file":[{"relation":"main_file","access_level":"open_access","content_type":"application/pdf","success":1,"checksum":"8b1d8f5ea20c8408acf466435fb6ae01","file_id":"12446","creator":"dernst","file_size":1098812,"date_updated":"2023-01-30T09:49:55Z","file_name":"2022_MolecularSystemsBio_Angermayr.pdf","date_created":"2023-01-30T09:49:55Z"}],"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"original","keyword":["Applied Mathematics","Computational Theory and Mathematics","General Agricultural and Biological Sciences","General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","Information Systems"],"status":"public","_id":"12261","department":[{"_id":"ToBo"}],"file_date_updated":"2023-01-30T09:49:55Z","date_updated":"2023-08-04T09:51:49Z","ddc":["570"],"oa":1,"quality_controlled":"1","publisher":"Embo Press","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.","date_created":"2023-01-16T09:58:34Z","doi":"10.15252/msb.202110490","date_published":"2022-09-01T00:00:00Z","year":"2022","isi":1,"has_accepted_license":"1","publication":"Molecular Systems Biology","day":"01","article_number":"e10490","article_processing_charge":"No","external_id":{"isi":["000856482800001"]},"author":[{"last_name":"Angermayr","full_name":"Angermayr, Andreas","orcid":"0000-0001-8619-2223","id":"4677C796-F248-11E8-B48F-1D18A9856A87","first_name":"Andreas"},{"first_name":"Tin Yau","full_name":"Pang, Tin Yau","last_name":"Pang"},{"first_name":"Guillaume","last_name":"Chevereau","full_name":"Chevereau, Guillaume"},{"id":"39B66846-F248-11E8-B48F-1D18A9856A87","first_name":"Karin","last_name":"Mitosch","full_name":"Mitosch, Karin"},{"last_name":"Lercher","full_name":"Lercher, Martin J","first_name":"Martin J"},{"last_name":"Bollenbach","full_name":"Bollenbach, Mark Tobias","orcid":"0000-0003-4398-476X","id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","first_name":"Mark Tobias"}],"title":"Growth‐mediated negative feedback shapes quantitative antibiotic response","citation":{"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.” Molecular Systems Biology. Embo Press, 2022. https://doi.org/10.15252/msb.202110490.","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.","mla":"Angermayr, Andreas, et al. “Growth‐mediated Negative Feedback Shapes Quantitative Antibiotic Response.” Molecular Systems Biology, vol. 18, no. 9, e10490, Embo Press, 2022, doi:10.15252/msb.202110490.","apa":"Angermayr, A., Pang, T. Y., Chevereau, G., Mitosch, K., Lercher, M. J., & Bollenbach, M. T. (2022). Growth‐mediated negative feedback shapes quantitative antibiotic response. Molecular Systems Biology. Embo Press. https://doi.org/10.15252/msb.202110490","ama":"Angermayr A, Pang TY, Chevereau G, Mitosch K, Lercher MJ, Bollenbach MT. Growth‐mediated negative feedback shapes quantitative antibiotic response. Molecular Systems Biology. 2022;18(9). doi:10.15252/msb.202110490","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,” Molecular Systems Biology, vol. 18, no. 9. Embo Press, 2022.","short":"A. Angermayr, T.Y. Pang, G. Chevereau, K. Mitosch, M.J. Lercher, M.T. Bollenbach, Molecular Systems Biology 18 (2022)."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8"},{"_id":"12288","status":"public","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"article_type":"original","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"ddc":["570"],"date_updated":"2023-08-04T10:29:48Z","department":[{"_id":"MaJö"},{"_id":"PeJo"}],"file_date_updated":"2023-01-30T11:50:53Z","pmid":1,"oa_version":"Published Version","acknowledged_ssus":[{"_id":"Bio"},{"_id":"PreCl"}],"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."}],"month":"09","intvolume":" 11","scopus_import":"1","file":[{"success":1,"file_id":"12463","checksum":"5a2a65e3e7225090c3d8199f3bbd7b7b","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"2022_eLife_Sumser.pdf","date_created":"2023-01-30T11:50:53Z","creator":"dernst","file_size":8506811,"date_updated":"2023-01-30T11:50:53Z"}],"language":[{"iso":"eng"}],"publication_identifier":{"eissn":["2050-084X"]},"publication_status":"published","volume":11,"ec_funded":1,"article_number":"79848","project":[{"call_identifier":"H2020","_id":"25B7EB9E-B435-11E9-9278-68D0E5697425","grant_number":"692692","name":"Biophysics and circuit function of a giant cortical glumatergic synapse"},{"name":"Circuits of Visual Attention","grant_number":"756502","call_identifier":"H2020","_id":"2634E9D2-B435-11E9-9278-68D0E5697425"},{"name":"The Wittgenstein Prize","grant_number":"Z00312","call_identifier":"FWF","_id":"25C5A090-B435-11E9-9278-68D0E5697425"},{"_id":"266D407A-B435-11E9-9278-68D0E5697425","name":"Neuronal networks of salience and spatial detection in the murine superior colliculus","grant_number":"LT000256"},{"grant_number":"ALTF 1098-2017","name":"Connecting sensory with motor processing in the superior colliculus","_id":"264FEA02-B435-11E9-9278-68D0E5697425"}],"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"chicago":"Sumser, Anton L, Maximilian A Jösch, Peter M Jonas, and Yoav Ben Simon. “Fast, High-Throughput Production of Improved Rabies Viral Vectors for Specific, Efficient and Versatile Transsynaptic Retrograde Labeling.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/elife.79848.","ista":"Sumser AL, Jösch MA, Jonas PM, Ben Simon Y. 2022. Fast, high-throughput production of improved rabies viral vectors for specific, efficient and versatile transsynaptic retrograde labeling. eLife. 11, 79848.","mla":"Sumser, Anton L., et al. “Fast, High-Throughput Production of Improved Rabies Viral Vectors for Specific, Efficient and Versatile Transsynaptic Retrograde Labeling.” ELife, vol. 11, 79848, eLife Sciences Publications, 2022, doi:10.7554/elife.79848.","ama":"Sumser AL, Jösch MA, Jonas PM, Ben Simon Y. Fast, high-throughput production of improved rabies viral vectors for specific, efficient and versatile transsynaptic retrograde labeling. eLife. 2022;11. doi:10.7554/elife.79848","apa":"Sumser, A. L., Jösch, M. A., Jonas, P. M., & Ben Simon, Y. (2022). Fast, high-throughput production of improved rabies viral vectors for specific, efficient and versatile transsynaptic retrograde labeling. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.79848","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,” eLife, vol. 11. eLife Sciences Publications, 2022."},"title":"Fast, high-throughput production of improved rabies viral vectors for specific, efficient and versatile transsynaptic retrograde labeling","author":[{"first_name":"Anton L","id":"3320A096-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-4792-1881","full_name":"Sumser, Anton L","last_name":"Sumser"},{"last_name":"Jösch","full_name":"Jösch, Maximilian A","orcid":"0000-0002-3937-1330","id":"2BD278E6-F248-11E8-B48F-1D18A9856A87","first_name":"Maximilian A"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","first_name":"Peter M","full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas"},{"last_name":"Ben Simon","full_name":"Ben Simon, Yoav","id":"43DF3136-F248-11E8-B48F-1D18A9856A87","first_name":"Yoav"}],"external_id":{"isi":["000892204300001"],"pmid":["36040301"]},"article_processing_charge":"No","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).","publisher":"eLife Sciences Publications","quality_controlled":"1","oa":1,"day":"15","publication":"eLife","isi":1,"has_accepted_license":"1","year":"2022","date_published":"2022-09-15T00:00:00Z","doi":"10.7554/elife.79848","date_created":"2023-01-16T10:04:15Z"},{"month":"12","intvolume":" 3","scopus_import":"1","oa_version":"Published Version","acknowledged_ssus":[{"_id":"Bio"}],"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"}],"volume":3,"issue":"4","related_material":{"record":[{"id":"11478","status":"public","relation":"other"}]},"license":"https://creativecommons.org/licenses/by-nc-nd/4.0/","ec_funded":1,"file":[{"success":1,"file_id":"12340","checksum":"3c71b8a60633d42c2f77c49025d5559b","relation":"main_file","access_level":"open_access","content_type":"application/pdf","file_name":"2022_STARProtocols_Huebschmann.pdf","date_created":"2023-01-23T09:50:51Z","creator":"dernst","file_size":6251945,"date_updated":"2023-01-23T09:50:51Z"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2666-1667"]},"publication_status":"published","status":"public","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Neuroscience"],"type":"journal_article","article_type":"letter_note","tmp":{"short":"CC BY-NC-ND (4.0)","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","image":"/images/cc_by_nc_nd.png"},"_id":"12117","file_date_updated":"2023-01-23T09:50:51Z","department":[{"_id":"SaSi"},{"_id":"GradSch"}],"ddc":["570"],"date_updated":"2023-11-02T12:21:32Z","publisher":"Elsevier","quality_controlled":"1","oa":1,"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_published":"2022-12-16T00:00:00Z","doi":"10.1016/j.xpro.2022.101866","date_created":"2023-01-12T11:56:38Z","day":"16","publication":"STAR Protocols","has_accepted_license":"1","year":"2022","project":[{"name":"Microglia action towards neuronal circuit formation and function in health and disease","grant_number":"715571","_id":"25D4A630-B435-11E9-9278-68D0E5697425","call_identifier":"H2020"},{"_id":"9B99D380-BA93-11EA-9121-9846C619BF3A","grant_number":"SC19-017","name":"How human microglia shape developing neurons during health and inflammation"}],"article_number":"101866","title":"Assessing human iPSC-derived microglia identity and function by immunostaining, phagocytosis, calcium activity, and inflammation assay","author":[{"full_name":"Hübschmann, Verena","last_name":"Hübschmann","first_name":"Verena","id":"32B7C918-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0003-4309-2251","full_name":"Korkut, Medina","last_name":"Korkut","id":"4B51CE74-F248-11E8-B48F-1D18A9856A87","first_name":"Medina"},{"last_name":"Siegert","orcid":"0000-0001-8635-0877","full_name":"Siegert, Sandra","first_name":"Sandra","id":"36ACD32E-F248-11E8-B48F-1D18A9856A87"}],"article_processing_charge":"No","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","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,” STAR Protocols, vol. 3, no. 4. Elsevier, 2022.","short":"V. Hübschmann, M. Korkut, S. Siegert, STAR Protocols 3 (2022).","ama":"Hübschmann V, Korkut M, Siegert S. Assessing human iPSC-derived microglia identity and function by immunostaining, phagocytosis, calcium activity, and inflammation assay. STAR Protocols. 2022;3(4). doi:10.1016/j.xpro.2022.101866","apa":"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. Elsevier. https://doi.org/10.1016/j.xpro.2022.101866","mla":"Hübschmann, Verena, et al. “Assessing Human IPSC-Derived Microglia Identity and Function by Immunostaining, Phagocytosis, Calcium Activity, and Inflammation Assay.” STAR Protocols, vol. 3, no. 4, 101866, Elsevier, 2022, doi:10.1016/j.xpro.2022.101866.","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.","chicago":"Hübschmann, Verena, Medina Korkut, and Sandra Siegert. “Assessing Human IPSC-Derived Microglia Identity and Function by Immunostaining, Phagocytosis, Calcium Activity, and Inflammation Assay.” STAR Protocols. Elsevier, 2022. https://doi.org/10.1016/j.xpro.2022.101866."}},{"article_number":"110729","title":"Two linked loci under mutation-selection balance and Muller’s ratchet","author":[{"last_name":"Khudiakova","full_name":"Khudiakova, Kseniia","orcid":"0000-0002-6246-1465","id":"4E6DC800-AE37-11E9-AC72-31CAE5697425","first_name":"Kseniia"},{"last_name":"Neretina","full_name":"Neretina, Tatiana Yu.","first_name":"Tatiana Yu."},{"first_name":"Alexey S.","last_name":"Kondrashov","full_name":"Kondrashov, Alexey S."}],"external_id":{"isi":["000659161500002"]},"article_processing_charge":"No","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"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.","chicago":"Khudiakova, Kseniia, Tatiana Yu. Neretina, and Alexey S. Kondrashov. “Two Linked Loci under Mutation-Selection Balance and Muller’s Ratchet.” Journal of Theoretical Biology. Elsevier , 2021. https://doi.org/10.1016/j.jtbi.2021.110729.","ama":"Khudiakova K, Neretina TY, Kondrashov AS. Two linked loci under mutation-selection balance and Muller’s ratchet. Journal of Theoretical Biology. 2021;524. doi:10.1016/j.jtbi.2021.110729","apa":"Khudiakova, K., Neretina, T. Y., & Kondrashov, A. S. (2021). Two linked loci under mutation-selection balance and Muller’s ratchet. Journal of Theoretical Biology. Elsevier . https://doi.org/10.1016/j.jtbi.2021.110729","ieee":"K. Khudiakova, T. Y. Neretina, and A. S. Kondrashov, “Two linked loci under mutation-selection balance and Muller’s ratchet,” Journal of Theoretical Biology, vol. 524. Elsevier , 2021.","short":"K. Khudiakova, T.Y. Neretina, A.S. Kondrashov, Journal of Theoretical Biology 524 (2021).","mla":"Khudiakova, Kseniia, et al. “Two Linked Loci under Mutation-Selection Balance and Muller’s Ratchet.” Journal of Theoretical Biology, vol. 524, 110729, Elsevier , 2021, doi:10.1016/j.jtbi.2021.110729."},"quality_controlled":"1","publisher":"Elsevier ","oa":1,"acknowledgement":"This work was supported by the Russian Science Foundation grant N 16-14-10173.","date_published":"2021-04-24T00:00:00Z","doi":"10.1016/j.jtbi.2021.110729","date_created":"2021-05-12T05:58:42Z","day":"24","publication":"Journal of Theoretical Biology","isi":1,"year":"2021","status":"public","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"],"article_type":"original","type":"journal_article","_id":"9387","department":[{"_id":"GradSch"}],"date_updated":"2023-08-08T13:32:40Z","month":"04","intvolume":" 524","main_file_link":[{"url":"https://www.biorxiv.org/content/10.1101/477489v1","open_access":"1"}],"oa_version":"Preprint","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."}],"volume":524,"language":[{"iso":"eng"}],"publication_identifier":{"issn":["0022-5193"]},"publication_status":"published"},{"_id":"10271","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"article_type":"original","type":"journal_article","keyword":["microbiology"],"status":"public","date_updated":"2023-08-14T11:43:23Z","ddc":["610"],"file_date_updated":"2021-11-11T10:54:40Z","abstract":[{"text":"Understanding interactions between antibiotics used in combination is an important theme in microbiology. Using the interactions between the antifolate drug trimethoprim and the ribosome-targeting antibiotic erythromycin in Escherichia coli as a model, we applied a transcriptomic approach for dissecting interactions between two antibiotics with different modes of action. When trimethoprim and erythromycin were combined, the transcriptional response of genes from the sulfate reduction pathway deviated from the dominant effect of trimethoprim on the transcriptome. We successfully altered the drug interaction from additivity to suppression by increasing the sulfate level in the growth environment and identified sulfate reduction as an important metabolic determinant that shapes the interaction between the two drugs. Our work highlights the potential of using prioritization of gene expression patterns as a tool for identifying key metabolic determinants that shape drug-drug interactions. We further demonstrated that the sigma factor-binding protein gene crl shapes the interactions between the two antibiotics, which provides a rare example of how naturally occurring variations between strains of the same bacterial species can sometimes generate very different drug interactions.","lang":"eng"}],"pmid":1,"oa_version":"Published Version","scopus_import":"1","intvolume":" 12","month":"10","publication_status":"published","publication_identifier":{"eissn":["1664-302X"]},"language":[{"iso":"eng"}],"file":[{"file_name":"2021_FrontiersMicrob_Qi.pdf","date_created":"2021-11-11T10:54:40Z","file_size":2397203,"date_updated":"2021-11-11T10:54:40Z","creator":"cchlebak","success":1,"checksum":"d41321748e9588dd3cf03e9a7222127f","file_id":"10272","content_type":"application/pdf","relation":"main_file","access_level":"open_access"}],"ec_funded":1,"volume":12,"article_number":"760017","project":[{"grant_number":"P27201-B22","name":"Revealing the mechanisms underlying drug interactions","call_identifier":"FWF","_id":"25E9AF9E-B435-11E9-9278-68D0E5697425"},{"call_identifier":"FP7","_id":"25E83C2C-B435-11E9-9278-68D0E5697425","name":"Optimality principles in responses to antibiotics","grant_number":"303507"}],"citation":{"short":"Q. Qi, S.A. Angermayr, M.T. Bollenbach, Frontiers in Microbiology 12 (2021).","ieee":"Q. Qi, S. A. Angermayr, and M. T. Bollenbach, “Uncovering Key Metabolic Determinants of the Drug Interactions Between Trimethoprim and Erythromycin in Escherichia coli,” Frontiers in Microbiology, vol. 12. Frontiers, 2021.","ama":"Qi Q, Angermayr SA, Bollenbach MT. Uncovering Key Metabolic Determinants of the Drug Interactions Between Trimethoprim and Erythromycin in Escherichia coli. Frontiers in Microbiology. 2021;12. doi:10.3389/fmicb.2021.760017","apa":"Qi, Q., Angermayr, S. A., & Bollenbach, M. T. (2021). Uncovering Key Metabolic Determinants of the Drug Interactions Between Trimethoprim and Erythromycin in Escherichia coli. Frontiers in Microbiology. Frontiers. https://doi.org/10.3389/fmicb.2021.760017","mla":"Qi, Qin, et al. “Uncovering Key Metabolic Determinants of the Drug Interactions Between Trimethoprim and Erythromycin in Escherichia Coli.” Frontiers in Microbiology, vol. 12, 760017, Frontiers, 2021, doi:10.3389/fmicb.2021.760017.","ista":"Qi Q, Angermayr SA, Bollenbach MT. 2021. Uncovering Key Metabolic Determinants of the Drug Interactions Between Trimethoprim and Erythromycin in Escherichia coli. Frontiers in Microbiology. 12, 760017.","chicago":"Qi, Qin, S. Andreas Angermayr, and Mark Tobias Bollenbach. “Uncovering Key Metabolic Determinants of the Drug Interactions Between Trimethoprim and Erythromycin in Escherichia Coli.” Frontiers in Microbiology. Frontiers, 2021. https://doi.org/10.3389/fmicb.2021.760017."},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","external_id":{"isi":["000715997300001"],"pmid":["34745067"]},"article_processing_charge":"No","author":[{"id":"3B22D412-F248-11E8-B48F-1D18A9856A87","first_name":"Qin","full_name":"Qi, Qin","orcid":"0000-0002-6148-2416","last_name":"Qi"},{"last_name":"Angermayr","full_name":"Angermayr, S. Andreas","first_name":"S. Andreas"},{"id":"3E6DB97A-F248-11E8-B48F-1D18A9856A87","first_name":"Mark Tobias","orcid":"0000-0003-4398-476X","full_name":"Bollenbach, Mark Tobias","last_name":"Bollenbach"}],"title":"Uncovering Key Metabolic Determinants of the Drug Interactions Between Trimethoprim and Erythromycin in Escherichia coli","acknowledgement":"High-throughput sequencing data were generated by the Vienna BioCenter Core Facilities. The authors would like to thank Karin Mitosch, Bor Kavcic, and Nadine Kraupner for their constructive feedback. The authors would also like to thank Gertraud Stift, Julia Flor, Renate Srsek, Agnieszka Wiktor, and Booshini Fernando for technical support.","oa":1,"quality_controlled":"1","publisher":"Frontiers","year":"2021","isi":1,"has_accepted_license":"1","publication":"Frontiers in Microbiology","day":"20","date_created":"2021-11-11T10:39:37Z","date_published":"2021-10-20T00:00:00Z","doi":"10.3389/fmicb.2021.760017"},{"volume":10,"file":[{"date_updated":"2021-11-18T07:02:02Z","file_size":2477302,"creator":"lgarciar","date_created":"2021-11-18T07:02:02Z","file_name":"elife-71575-v1.pdf","content_type":"application/pdf","access_level":"open_access","relation":"main_file","file_id":"10302","checksum":"59318e9e41507cec83c2f4070e6ad540","success":1}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["2050-084X"]},"publication_status":"published","month":"11","intvolume":" 10","oa_version":"Published Version","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."}],"file_date_updated":"2021-11-18T07:02:02Z","department":[{"_id":"GaNo"}],"ddc":["570"],"date_updated":"2023-08-14T11:50:50Z","status":"public","keyword":["general immunology and microbiology","general biochemistry","genetics and molecular biology","general medicine","general neuroscience"],"article_type":"original","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"_id":"10301","doi":"10.7554/elife.71575","date_published":"2021-11-17T00:00:00Z","date_created":"2021-11-18T06:59:45Z","day":"17","publication":"eLife","isi":1,"has_accepted_license":"1","year":"2021","publisher":"eLife Sciences Publications","quality_controlled":"1","oa":1,"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).","title":"Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly","author":[{"last_name":"Conde-Dusman","full_name":"Conde-Dusman, María J","first_name":"María J"},{"last_name":"Dey","full_name":"Dey, Partha N","first_name":"Partha N"},{"first_name":"Óscar","full_name":"Elía-Zudaire, Óscar","last_name":"Elía-Zudaire"},{"last_name":"Garcia Rabaneda","full_name":"Garcia Rabaneda, Luis E","first_name":"Luis E","id":"33D1B084-F248-11E8-B48F-1D18A9856A87"},{"full_name":"García-Lira, Carmen","last_name":"García-Lira","first_name":"Carmen"},{"full_name":"Grand, Teddy","last_name":"Grand","first_name":"Teddy"},{"first_name":"Victor","last_name":"Briz","full_name":"Briz, Victor"},{"full_name":"Velasco, Eric R","last_name":"Velasco","first_name":"Eric R"},{"first_name":"Raül","full_name":"Andero Galí, Raül","last_name":"Andero Galí"},{"full_name":"Niñerola, Sergio","last_name":"Niñerola","first_name":"Sergio"},{"full_name":"Barco, Angel","last_name":"Barco","first_name":"Angel"},{"full_name":"Paoletti, Pierre","last_name":"Paoletti","first_name":"Pierre"},{"first_name":"John F","last_name":"Wesseling","full_name":"Wesseling, John F"},{"first_name":"Fabrizio","full_name":"Gardoni, Fabrizio","last_name":"Gardoni"},{"first_name":"Steven J","last_name":"Tavalin","full_name":"Tavalin, Steven J"},{"first_name":"Isabel","last_name":"Perez-Otaño","full_name":"Perez-Otaño, Isabel"}],"article_processing_charge":"No","external_id":{"isi":["000720945900001"]},"user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","citation":{"mla":"Conde-Dusman, María J., et al. “Control of Protein Synthesis and Memory by GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1 Assembly.” ELife, vol. 10, e71575, eLife Sciences Publications, 2021, doi:10.7554/elife.71575.","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. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.71575","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. eLife. 2021;10. doi:10.7554/elife.71575","ieee":"M. J. Conde-Dusman et al., “Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly,” eLife, vol. 10. eLife Sciences Publications, 2021.","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).","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.” ELife. eLife Sciences Publications, 2021. https://doi.org/10.7554/elife.71575.","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."},"article_number":"e71575"},{"date_published":"2020-09-08T00:00:00Z","doi":"10.7554/elife.54383","date_created":"2022-04-07T07:43:48Z","has_accepted_license":"1","year":"2020","day":"08","publication":"eLife","publisher":"eLife Sciences Publications","quality_controlled":"1","oa":1,"author":[{"full_name":"Bersini, Simone","last_name":"Bersini","first_name":"Simone"},{"last_name":"Schulte","full_name":"Schulte, Roberta","first_name":"Roberta"},{"first_name":"Ling","full_name":"Huang, Ling","last_name":"Huang"},{"first_name":"Hannah","last_name":"Tsai","full_name":"Tsai, Hannah"},{"full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X","last_name":"HETZER","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","first_name":"Martin W"}],"external_id":{"pmid":["32896271"]},"article_processing_charge":"No","title":"Direct reprogramming of human smooth muscle and vascular endothelial cells reveals defects associated with aging and Hutchinson-Gilford progeria syndrome","citation":{"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.” ELife, vol. 9, e54383, eLife Sciences Publications, 2020, doi:10.7554/elife.54383.","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. eLife. 2020;9. doi:10.7554/elife.54383","apa":"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. eLife Sciences Publications. https://doi.org/10.7554/elife.54383","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,” eLife, 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.” ELife. eLife Sciences Publications, 2020. https://doi.org/10.7554/elife.54383.","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."},"user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","article_number":"e54383","volume":9,"publication_identifier":{"issn":["2050-084X"]},"publication_status":"published","file":[{"date_updated":"2022-04-08T06:53:10Z","file_size":4399825,"creator":"dernst","date_created":"2022-04-08T06:53:10Z","file_name":"2020_eLife_Bersini.pdf","content_type":"application/pdf","access_level":"open_access","relation":"main_file","file_id":"11132","checksum":"f8b3821349a194050be02570d8fe7d4b","success":1}],"language":[{"iso":"eng"}],"scopus_import":"1","month":"09","intvolume":" 9","abstract":[{"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.","lang":"eng"}],"pmid":1,"oa_version":"Published Version","file_date_updated":"2022-04-08T06:53:10Z","date_updated":"2022-07-18T08:30:37Z","extern":"1","ddc":["570"],"type":"journal_article","article_type":"original","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"status":"public","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"_id":"11055"},{"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."}],"oa_version":"Published Version","scopus_import":"1","main_file_link":[{"open_access":"1","url":"https://doi.org/10.7554/eLife.55275"}],"month":"02","intvolume":" 9","publication_identifier":{"issn":["2050-084X"]},"publication_status":"published","language":[{"iso":"eng"}],"volume":9,"_id":"15153","type":"journal_article","article_type":"original","status":"public","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"date_updated":"2024-03-25T12:25:02Z","extern":"1","quality_controlled":"1","publisher":"eLife Sciences Publications","oa":1,"year":"2020","day":"26","publication":"eLife","date_published":"2020-02-26T00:00:00Z","doi":"10.7554/elife.55275","date_created":"2024-03-21T07:55:12Z","article_number":"55275","citation":{"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.” ELife. eLife Sciences Publications, 2020. https://doi.org/10.7554/elife.55275.","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.","mla":"Fribourgh, Jennifer L., et al. “Dynamics at the Serine Loop Underlie Differential Affinity of Cryptochromes for CLOCK:BMAL1 to Control Circadian Timing.” ELife, vol. 9, 55275, eLife Sciences Publications, 2020, doi:10.7554/elife.55275.","ieee":"J. L. Fribourgh et al., “Dynamics at the serine loop underlie differential affinity of cryptochromes for CLOCK:BMAL1 to control circadian timing,” eLife, vol. 9. eLife Sciences Publications, 2020.","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).","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. eLife. 2020;9. doi:10.7554/elife.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. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.55275"},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","author":[{"last_name":"Fribourgh","full_name":"Fribourgh, Jennifer L","first_name":"Jennifer L"},{"last_name":"Srivastava","full_name":"Srivastava, Ashutosh","first_name":"Ashutosh"},{"last_name":"Sandate","full_name":"Sandate, Colby R","first_name":"Colby R"},{"last_name":"Michael","full_name":"Michael, Alicia Kathleen","id":"6437c950-2a03-11ee-914d-d6476dd7b75c","first_name":"Alicia Kathleen"},{"last_name":"Hsu","full_name":"Hsu, Peter L","first_name":"Peter L"},{"full_name":"Rakers, Christin","last_name":"Rakers","first_name":"Christin"},{"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","full_name":"Parico, Gian Carlo G","first_name":"Gian Carlo G"},{"first_name":"Sarvind","full_name":"Tripathi, Sarvind","last_name":"Tripathi"},{"last_name":"Zheng","full_name":"Zheng, Ning","first_name":"Ning"},{"first_name":"Gabriel C","full_name":"Lander, Gabriel C","last_name":"Lander"},{"full_name":"Hirota, Tsuyoshi","last_name":"Hirota","first_name":"Tsuyoshi"},{"last_name":"Tama","full_name":"Tama, Florence","first_name":"Florence"},{"last_name":"Partch","full_name":"Partch, Carrie L","first_name":"Carrie L"}],"article_processing_charge":"No","title":"Dynamics at the serine loop underlie differential affinity of cryptochromes for CLOCK:BMAL1 to control circadian timing"},{"article_number":"42530","title":"Natural depletion of histone H1 in sex cells causes DNA demethylation, heterochromatin decondensation and transposon activation","external_id":{"unknown":["31135340"]},"article_processing_charge":"No","author":[{"first_name":"Shengbo","full_name":"He, Shengbo","last_name":"He"},{"full_name":"Vickers, Martin","last_name":"Vickers","first_name":"Martin"},{"full_name":"Zhang, Jingyi","last_name":"Zhang","first_name":"Jingyi"},{"orcid":"0000-0002-4008-1234","full_name":"Feng, Xiaoqi","last_name":"Feng","first_name":"Xiaoqi","id":"e0164712-22ee-11ed-b12a-d80fcdf35958"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"mla":"He, Shengbo, et al. “Natural Depletion of Histone H1 in Sex Cells Causes DNA Demethylation, Heterochromatin Decondensation and Transposon Activation.” ELife, vol. 8, 42530, eLife Sciences Publications, Ltd, 2019, doi:10.7554/elife.42530.","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,” eLife, vol. 8. eLife Sciences Publications, Ltd, 2019.","short":"S. He, M. Vickers, J. Zhang, X. Feng, ELife 8 (2019).","apa":"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. eLife Sciences Publications, Ltd. https://doi.org/10.7554/elife.42530","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. eLife. 2019;8. doi:10.7554/elife.42530","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.” ELife. eLife Sciences Publications, Ltd, 2019. https://doi.org/10.7554/elife.42530.","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."},"oa":1,"publisher":"eLife Sciences Publications, Ltd","quality_controlled":"1","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","date_published":"2019-05-28T00:00:00Z","doi":"10.7554/elife.42530","publication":"eLife","day":"28","year":"2019","has_accepted_license":"1","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"article_type":"original","type":"journal_article","_id":"12192","file_date_updated":"2023-02-07T09:42:46Z","department":[{"_id":"XiFe"}],"ddc":["580"],"extern":"1","date_updated":"2023-05-08T10:54:12Z","intvolume":" 8","month":"05","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6594752/","open_access":"1"}],"scopus_import":"1","oa_version":"Published Version","abstract":[{"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.","lang":"eng"}],"volume":8,"language":[{"iso":"eng"}],"file":[{"date_created":"2023-02-07T09:42:46Z","file_name":"2019_elife_He.pdf","date_updated":"2023-02-07T09:42:46Z","file_size":2493837,"creator":"alisjak","file_id":"12525","checksum":"ea6b89c20d59e5eb3646916fe5d568ad","success":1,"content_type":"application/pdf","access_level":"open_access","relation":"main_file"}],"publication_status":"published","publication_identifier":{"issn":["2050-084X"]}},{"intvolume":" 8","month":"10","scopus_import":"1","pmid":1,"oa_version":"Published Version","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."}],"volume":8,"related_material":{"record":[{"relation":"research_data","status":"public","id":"13079"}]},"language":[{"iso":"eng"}],"file":[{"date_created":"2022-04-08T08:18:01Z","file_name":"2019_eLife_Buchwalter.pdf","creator":"dernst","date_updated":"2022-04-08T08:18:01Z","file_size":6984654,"file_id":"11138","checksum":"1e8672a1e9c3dc0a2d3d0dad89673616","success":1,"access_level":"open_access","relation":"main_file","content_type":"application/pdf"}],"publication_status":"published","publication_identifier":{"issn":["2050-084X"]},"keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"original","_id":"11060","file_date_updated":"2022-04-08T08:18:01Z","ddc":["570"],"extern":"1","date_updated":"2023-05-31T06:36:22Z","oa":1,"publisher":"eLife Sciences Publications","quality_controlled":"1","date_created":"2022-04-07T07:45:02Z","doi":"10.7554/elife.49796","date_published":"2019-10-10T00:00:00Z","publication":"eLife","day":"10","year":"2019","has_accepted_license":"1","article_number":"e49796","title":"Selective clearance of the inner nuclear membrane protein emerin by vesicular transport during ER stress","article_processing_charge":"No","external_id":{"pmid":["31599721"]},"author":[{"first_name":"Abigail","full_name":"Buchwalter, Abigail","last_name":"Buchwalter"},{"first_name":"Roberta","full_name":"Schulte, Roberta","last_name":"Schulte"},{"first_name":"Hsiao","last_name":"Tsai","full_name":"Tsai, Hsiao"},{"first_name":"Juliana","last_name":"Capitanio","full_name":"Capitanio, Juliana"},{"full_name":"HETZER, Martin W","orcid":"0000-0002-2111-992X","last_name":"HETZER","first_name":"Martin W","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed"}],"user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","citation":{"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.” ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/elife.49796.","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.","mla":"Buchwalter, Abigail, et al. “Selective Clearance of the Inner Nuclear Membrane Protein Emerin by Vesicular Transport during ER Stress.” ELife, vol. 8, e49796, eLife Sciences Publications, 2019, doi:10.7554/elife.49796.","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,” eLife, vol. 8. eLife Sciences Publications, 2019.","short":"A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, M. Hetzer, ELife 8 (2019).","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. eLife. 2019;8. doi:10.7554/elife.49796","apa":"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. eLife Sciences Publications. https://doi.org/10.7554/elife.49796"}},{"article_number":"e30292","article_processing_charge":"No","external_id":{"pmid":["29119945"]},"author":[{"first_name":"Sebastian Carsten Johannes","full_name":"Helle, Sebastian Carsten Johannes","last_name":"Helle"},{"first_name":"Qian","last_name":"Feng","full_name":"Feng, Qian"},{"full_name":"Aebersold, Mathias J","last_name":"Aebersold","first_name":"Mathias J"},{"first_name":"Luca","full_name":"Hirt, Luca","last_name":"Hirt"},{"full_name":"Grüter, Raphael R","last_name":"Grüter","first_name":"Raphael R"},{"full_name":"Vahid, Afshin","last_name":"Vahid","first_name":"Afshin"},{"first_name":"Andrea","full_name":"Sirianni, Andrea","last_name":"Sirianni"},{"first_name":"Serge","full_name":"Mostowy, Serge","last_name":"Mostowy"},{"full_name":"Snedeker, Jess G","last_name":"Snedeker","first_name":"Jess G"},{"last_name":"Šarić","orcid":"0000-0002-7854-2139","full_name":"Šarić, Anđela","first_name":"Anđela","id":"bf63d406-f056-11eb-b41d-f263a6566d8b"},{"first_name":"Timon","last_name":"Idema","full_name":"Idema, Timon"},{"last_name":"Zambelli","full_name":"Zambelli, Tomaso","first_name":"Tomaso"},{"first_name":"Benoît","full_name":"Kornmann, Benoît","last_name":"Kornmann"}],"title":"Mechanical force induces mitochondrial fission","citation":{"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.","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.” ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/elife.30292.","ama":"Helle SCJ, Feng Q, Aebersold MJ, et al. Mechanical force induces mitochondrial fission. eLife. 2017;6. doi:10.7554/elife.30292","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. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.30292","ieee":"S. C. J. Helle et al., “Mechanical force induces mitochondrial fission,” eLife, 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).","mla":"Helle, Sebastian Carsten Johannes, et al. “Mechanical Force Induces Mitochondrial Fission.” ELife, vol. 6, e30292, eLife Sciences Publications, 2017, doi:10.7554/elife.30292."},"user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","oa":1,"quality_controlled":"1","publisher":"eLife Sciences Publications","date_created":"2021-11-29T08:51:38Z","date_published":"2017-11-09T00:00:00Z","doi":"10.7554/elife.30292","year":"2017","has_accepted_license":"1","publication":"eLife","day":"09","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"article_type":"original","type":"journal_article","keyword":["general immunology and microbiology","general biochemistry","genetics and molecular biology","general medicine","general neuroscience"],"status":"public","_id":"10370","file_date_updated":"2021-11-29T09:07:41Z","date_updated":"2021-11-29T09:28:14Z","ddc":["572"],"extern":"1","main_file_link":[{"open_access":"1","url":"https://elifesciences.org/articles/30292"}],"scopus_import":"1","intvolume":" 6","month":"11","abstract":[{"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.","lang":"eng"}],"oa_version":"Published Version","pmid":1,"volume":6,"publication_status":"published","publication_identifier":{"issn":["2050-084X"]},"language":[{"iso":"eng"}],"file":[{"date_created":"2021-11-29T09:07:41Z","file_name":"2017_eLife_Helle.pdf","creator":"cchlebak","date_updated":"2021-11-29T09:07:41Z","file_size":6120157,"checksum":"c35f42dcfb007f6d6c761a27e24c26d3","file_id":"10372","success":1,"access_level":"open_access","relation":"main_file","content_type":"application/pdf"}]},{"extern":"1","date_updated":"2023-11-07T12:36:20Z","_id":"14286","status":"public","keyword":["Applied Microbiology and Biotechnology","Bioengineering","Biotechnology"],"type":"journal_article","article_type":"original","language":[{"iso":"eng"}],"publication_identifier":{"issn":["0006-3592"]},"publication_status":"published","volume":114,"issue":"4","oa_version":"None","pmid":1,"abstract":[{"text":"The bacteriophage M13 has found frequent applications in nanobiotechnology due to its chemically and genetically tunable protein surface and its ability to self-assemble into colloidal membranes. Additionally, its single-stranded (ss) genome is commonly used as scaffold for DNA origami. Despite the manifold uses of M13, upstream production methods for phage and scaffold ssDNA are underexamined with respect to future industrial usage. Here, the high-cell-density phage production with Escherichia coli as host organism was studied in respect of medium composition, infection time, multiplicity of infection, and specific growth rate. The specific growth rate and the multiplicity of infection were identified as the crucial state variables that influence phage amplification rate on one hand and the concentration of produced ssDNA on the other hand. Using a growth rate of 0.15 h−1 and a multiplicity of infection of 0.05 pfu cfu−1 in the fed-batch production process, the concentration of pure isolated M13 ssDNA usable for scaffolded DNA origami could be enhanced by 54% to 590 mg L−1. Thus, our results help enabling M13 production for industrial uses in nanobiotechnology. Biotechnol. Bioeng. 2017;114: 777–784.","lang":"eng"}],"month":"04","intvolume":" 114","scopus_import":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"ista":"Kick B, Hensler S, Praetorius FM, Dietz H, Weuster-Botz D. 2017. Specific growth rate and multiplicity of infection affect high-cell-density fermentation with bacteriophage M13 for ssDNA production. Biotechnology and Bioengineering. 114(4), 777–784.","chicago":"Kick, Benjamin, Samantha Hensler, Florian M Praetorius, Hendrik Dietz, and Dirk Weuster-Botz. “Specific Growth Rate and Multiplicity of Infection Affect High-Cell-Density Fermentation with Bacteriophage M13 for SsDNA Production.” Biotechnology and Bioengineering. Wiley, 2017. https://doi.org/10.1002/bit.26200.","ieee":"B. Kick, S. Hensler, F. M. Praetorius, H. Dietz, and D. Weuster-Botz, “Specific growth rate and multiplicity of infection affect high-cell-density fermentation with bacteriophage M13 for ssDNA production,” Biotechnology and Bioengineering, vol. 114, no. 4. Wiley, pp. 777–784, 2017.","short":"B. Kick, S. Hensler, F.M. Praetorius, H. Dietz, D. Weuster-Botz, Biotechnology and Bioengineering 114 (2017) 777–784.","apa":"Kick, B., Hensler, S., Praetorius, F. M., Dietz, H., & Weuster-Botz, D. (2017). Specific growth rate and multiplicity of infection affect high-cell-density fermentation with bacteriophage M13 for ssDNA production. Biotechnology and Bioengineering. Wiley. https://doi.org/10.1002/bit.26200","ama":"Kick B, Hensler S, Praetorius FM, Dietz H, Weuster-Botz D. Specific growth rate and multiplicity of infection affect high-cell-density fermentation with bacteriophage M13 for ssDNA production. Biotechnology and Bioengineering. 2017;114(4):777-784. doi:10.1002/bit.26200","mla":"Kick, Benjamin, et al. “Specific Growth Rate and Multiplicity of Infection Affect High-Cell-Density Fermentation with Bacteriophage M13 for SsDNA Production.” Biotechnology and Bioengineering, vol. 114, no. 4, Wiley, 2017, pp. 777–84, doi:10.1002/bit.26200."},"title":"Specific growth rate and multiplicity of infection affect high-cell-density fermentation with bacteriophage M13 for ssDNA production","author":[{"last_name":"Kick","full_name":"Kick, Benjamin","first_name":"Benjamin"},{"last_name":"Hensler","full_name":"Hensler, Samantha","first_name":"Samantha"},{"full_name":"Praetorius, Florian M","last_name":"Praetorius","first_name":"Florian M","id":"dfec9381-4341-11ee-8fd8-faa02bba7d62"},{"full_name":"Dietz, Hendrik","last_name":"Dietz","first_name":"Hendrik"},{"full_name":"Weuster-Botz, Dirk","last_name":"Weuster-Botz","first_name":"Dirk"}],"external_id":{"pmid":["27748519"]},"article_processing_charge":"No","day":"01","publication":"Biotechnology and Bioengineering","year":"2017","doi":"10.1002/bit.26200","date_published":"2017-04-01T00:00:00Z","date_created":"2023-09-06T12:08:29Z","page":"777-784","publisher":"Wiley","quality_controlled":"1"},{"extern":"1","date_updated":"2024-03-25T12:22:54Z","_id":"15154","status":"public","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"type":"journal_article","article_type":"original","language":[{"iso":"eng"}],"publication_identifier":{"issn":["2050-084X"]},"publication_status":"published","volume":6,"pmid":1,"oa_version":"Published Version","abstract":[{"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.","lang":"eng"}],"month":"08","intvolume":" 6","scopus_import":"1","main_file_link":[{"url":"https://doi.org/10.7554/eLife.26163","open_access":"1"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"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.” ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/elife.26163.","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.” ELife, vol. 6, 26163, eLife Sciences Publications, 2017, doi:10.7554/elife.26163.","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).","ieee":"J. C. Fong et al., “Structural dynamics of RbmA governs plasticity of Vibrio cholerae biofilms,” eLife, vol. 6. eLife Sciences Publications, 2017.","ama":"Fong JC, Rogers A, Michael AK, et al. Structural dynamics of RbmA governs plasticity of Vibrio cholerae biofilms. eLife. 2017;6. doi:10.7554/elife.26163","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. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.26163"},"title":"Structural dynamics of RbmA governs plasticity of Vibrio cholerae biofilms","author":[{"first_name":"Jiunn CN","last_name":"Fong","full_name":"Fong, Jiunn CN"},{"first_name":"Andrew","full_name":"Rogers, Andrew","last_name":"Rogers"},{"id":"6437c950-2a03-11ee-914d-d6476dd7b75c","first_name":"Alicia Kathleen","last_name":"Michael","full_name":"Michael, Alicia Kathleen"},{"last_name":"Parsley","full_name":"Parsley, Nicole C","first_name":"Nicole C"},{"last_name":"Cornell","full_name":"Cornell, William-Cole","first_name":"William-Cole"},{"first_name":"Yu-Cheng","full_name":"Lin, Yu-Cheng","last_name":"Lin"},{"first_name":"Praveen K","last_name":"Singh","full_name":"Singh, Praveen K"},{"last_name":"Hartmann","full_name":"Hartmann, Raimo","first_name":"Raimo"},{"full_name":"Drescher, Knut","last_name":"Drescher","first_name":"Knut"},{"last_name":"Vinogradov","full_name":"Vinogradov, Evgeny","first_name":"Evgeny"},{"full_name":"Dietrich, Lars EP","last_name":"Dietrich","first_name":"Lars EP"},{"first_name":"Carrie L","full_name":"Partch, Carrie L","last_name":"Partch"},{"full_name":"Yildiz, Fitnat H","last_name":"Yildiz","first_name":"Fitnat H"}],"article_processing_charge":"Yes","external_id":{"pmid":["28762945"]},"article_number":"26163","day":"01","publication":"eLife","year":"2017","doi":"10.7554/elife.26163","date_published":"2017-08-01T00:00:00Z","date_created":"2024-03-21T07:55:36Z","quality_controlled":"1","publisher":"eLife Sciences Publications","oa":1}]