[{"page":"830-842","date_created":"2022-03-04T08:32:36Z","month":"12","publisher":"Springer Nature","intvolume":"         1","status":"public","publication":"Nature Computational Science","department":[{"_id":"PeJo"}],"quality_controlled":"1","title":"How connectivity rules and synaptic properties shape the efficacy of pattern separation in the entorhinal cortex–dentate gyrus–CA3 network","citation":{"apa":"Guzmán, J., Schlögl, A., Espinoza Martinez, C., Zhang, X., Suter, B., &#38; Jonas, P. M. (2021). How connectivity rules and synaptic properties shape the efficacy of pattern separation in the entorhinal cortex–dentate gyrus–CA3 network. <i>Nature Computational Science</i>. Springer Nature. <a href=\"https://doi.org/10.1038/s43588-021-00157-1\">https://doi.org/10.1038/s43588-021-00157-1</a>","ama":"Guzmán J, Schlögl A, Espinoza Martinez C, Zhang X, Suter B, Jonas PM. How connectivity rules and synaptic properties shape the efficacy of pattern separation in the entorhinal cortex–dentate gyrus–CA3 network. <i>Nature Computational Science</i>. 2021;1(12):830-842. doi:<a href=\"https://doi.org/10.1038/s43588-021-00157-1\">10.1038/s43588-021-00157-1</a>","short":"J. Guzmán, A. Schlögl, C. Espinoza Martinez, X. Zhang, B. Suter, P.M. Jonas, Nature Computational Science 1 (2021) 830–842.","mla":"Guzmán, José, et al. “How Connectivity Rules and Synaptic Properties Shape the Efficacy of Pattern Separation in the Entorhinal Cortex–Dentate Gyrus–CA3 Network.” <i>Nature Computational Science</i>, vol. 1, no. 12, Springer Nature, 2021, pp. 830–42, doi:<a href=\"https://doi.org/10.1038/s43588-021-00157-1\">10.1038/s43588-021-00157-1</a>.","ista":"Guzmán J, Schlögl A, Espinoza Martinez C, Zhang X, Suter B, Jonas PM. 2021. How connectivity rules and synaptic properties shape the efficacy of pattern separation in the entorhinal cortex–dentate gyrus–CA3 network. Nature Computational Science. 1(12), 830–842.","ieee":"J. Guzmán, A. Schlögl, C. Espinoza Martinez, X. Zhang, B. Suter, and P. M. Jonas, “How connectivity rules and synaptic properties shape the efficacy of pattern separation in the entorhinal cortex–dentate gyrus–CA3 network,” <i>Nature Computational Science</i>, vol. 1, no. 12. Springer Nature, pp. 830–842, 2021.","chicago":"Guzmán, José, Alois Schlögl, Claudia  Espinoza Martinez, Xiaomin Zhang, Benjamin Suter, and Peter M Jonas. “How Connectivity Rules and Synaptic Properties Shape the Efficacy of Pattern Separation in the Entorhinal Cortex–Dentate Gyrus–CA3 Network.” <i>Nature Computational Science</i>. Springer Nature, 2021. <a href=\"https://doi.org/10.1038/s43588-021-00157-1\">https://doi.org/10.1038/s43588-021-00157-1</a>."},"ec_funded":1,"author":[{"last_name":"Guzmán","first_name":"José","full_name":"Guzmán, José","id":"30CC5506-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2209-5242"},{"orcid":"0000-0002-5621-8100","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87","first_name":"Alois","full_name":"Schlögl, Alois","last_name":"Schlögl"},{"last_name":"Espinoza Martinez","full_name":"Espinoza Martinez, Claudia ","first_name":"Claudia ","id":"31FFEE2E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-4710-2082"},{"last_name":"Zhang","full_name":"Zhang, Xiaomin","first_name":"Xiaomin","id":"423EC9C2-F248-11E8-B48F-1D18A9856A87"},{"id":"4952F31E-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-9885-6936","full_name":"Suter, Benjamin","first_name":"Benjamin","last_name":"Suter"},{"first_name":"Peter M","full_name":"Jonas, Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804"}],"type":"journal_article","day":"16","related_material":{"link":[{"url":"https://ista.ac.at/en/news/spot-the-difference/","relation":"press_release"}],"record":[{"id":"10110","relation":"software","status":"public"}]},"project":[{"_id":"25B7EB9E-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","name":"Biophysics and circuit function of a giant cortical glumatergic synapse","grant_number":"692692"},{"_id":"25C5A090-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"Z00312","name":"The Wittgenstein Prize"}],"acknowledgement":"We thank A. Aertsen, N. Kopell, W. Maass, A. Roth, F. Stella and T. Vogels for critically reading earlier versions of the manuscript. We are grateful to F. Marr and C. Altmutter for excellent technical assistance, E. Kralli-Beller for manuscript editing, and the Scientific Service Units of IST Austria for efficient support. Finally, we thank T. Carnevale, L. Erdös, M. Hines, D. Nykamp and D. Schröder for useful discussions, and R. Friedrich and S. Wiechert for sharing unpublished data. This project received funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement no. 692692, P.J.) and the Fond zur Förderung der Wissenschaftlichen Forschung (Z 312-B27, Wittgenstein award to P.J. and P 31815 to S.J.G.).","doi":"10.1038/s43588-021-00157-1","ddc":["610"],"keyword":["general medicine"],"language":[{"iso":"eng"}],"article_processing_charge":"No","issue":"12","_id":"10816","date_published":"2021-12-16T00:00:00Z","abstract":[{"text":"Pattern separation is a fundamental brain computation that converts small differences in input patterns into large differences in output patterns. Several synaptic mechanisms of pattern separation have been proposed, including code expansion, inhibition and plasticity; however, which of these mechanisms play a role in the entorhinal cortex (EC)–dentate gyrus (DG)–CA3 circuit, a classical pattern separation circuit, remains unclear. Here we show that a biologically realistic, full-scale EC–DG–CA3 circuit model, including granule cells (GCs) and parvalbumin-positive inhibitory interneurons (PV+-INs) in the DG, is an efficient pattern separator. Both external gamma-modulated inhibition and internal lateral inhibition mediated by PV+-INs substantially contributed to pattern separation. Both local connectivity and fast signaling at GC–PV+-IN synapses were important for maximum effectiveness. Similarly, mossy fiber synapses with conditional detonator properties contributed to pattern separation. By contrast, perforant path synapses with Hebbian synaptic plasticity and direct EC–CA3 connection shifted the network towards pattern completion. Our results demonstrate that the specific properties of cells and synapses optimize higher-order computations in biological networks and might be useful to improve the deep learning capabilities of technical networks.","lang":"eng"}],"file":[{"checksum":"9fec5b667909ef52be96d502e4f8c2ae","access_level":"open_access","date_updated":"2022-06-18T22:30:03Z","file_size":1699466,"creator":"patrickd","file_name":"Guzmanetal2021.pdf","embargo":"2022-06-17","date_created":"2022-06-02T12:51:07Z","file_id":"11430","relation":"main_file","content_type":"application/pdf"},{"embargo":"2022-06-17","file_name":"Guzmanetal2021Suppl.pdf","file_size":3005651,"creator":"patrickd","date_updated":"2022-06-18T22:30:03Z","access_level":"open_access","checksum":"52a005b13a114e3c3a28fa6bbe8b1a8d","content_type":"application/pdf","file_id":"11431","relation":"supplementary_material","title":"Supplementary Material","date_created":"2022-06-02T12:53:47Z"}],"oa":1,"main_file_link":[{"url":"https://www.biorxiv.org/content/10.1101/647800","open_access":"1"}],"publication_status":"published","volume":1,"file_date_updated":"2022-06-18T22:30:03Z","year":"2021","oa_version":"Submitted Version","has_accepted_license":"1","article_type":"original","acknowledged_ssus":[{"_id":"SSU"}],"publication_identifier":{"issn":["2662-8457"]},"scopus_import":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2023-08-10T22:30:10Z"},{"status":"public","intvolume":"       303","quality_controlled":"1","department":[{"_id":"JiFr"},{"_id":"Bio"}],"publication":"Plant Science","isi":1,"publisher":"Elsevier","date_created":"2020-12-09T14:48:28Z","month":"02","ddc":["580"],"doi":"10.1016/j.plantsci.2020.110750","language":[{"iso":"eng"}],"keyword":["Agronomy and Crop Science","Plant Science","Genetics","General Medicine"],"acknowledgement":"We would like to acknowledge Bioimaging and Life Science Facilities at IST Austria for continuous support and also the Plant Sciences Core Facility of CEITEC Masaryk University for their support with obtaining a part of the scientific data. We gratefully acknowledge Lindy Abas for help with ABP1::GFP-ABP1 construct design. This project has received funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation program [grant agreement no. 742985] and Austrian Science Fund (FWF) [I 3630-B25] to J.F.; DOC Fellowship of the Austrian Academy of Sciences to L.L.; the European Structural and Investment Funds, Operational Programme Research, Development and Education - Project „MSCAfellow@MUNI“ [CZ.02.2.69/0.0/0.0/17_050/0008496] to M.P.. This project was also supported by the Czech Science Foundation [GA 20-20860Y] to M.Z and MEYS CR [project no.CZ.02.1.01/0.0/0.0/16_019/0000738] to M. Č.","pmid":1,"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"},{"_id":"26B4D67E-B435-11E9-9278-68D0E5697425","name":"A Case Study of Plant Growth Regulation: Molecular Mechanism of Auxin-mediated Rapid Growth Inhibition in Arabidopsis Root","grant_number":"25351"}],"related_material":{"record":[{"relation":"dissertation_contains","id":"11626","status":"public"},{"status":"public","relation":"dissertation_contains","id":"10083"}]},"author":[{"last_name":"Gelová","full_name":"Gelová, Zuzana","first_name":"Zuzana","orcid":"0000-0003-4783-1752","id":"0AE74790-0E0B-11E9-ABC7-1ACFE5697425"},{"id":"35A03822-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-1286-7368","first_name":"Michelle C","full_name":"Gallei, Michelle C","last_name":"Gallei"},{"first_name":"Markéta","full_name":"Pernisová, Markéta","last_name":"Pernisová"},{"first_name":"Géraldine","full_name":"Brunoud, Géraldine","last_name":"Brunoud"},{"id":"61A66458-47E9-11EA-85BA-8AEAAF14E49A","orcid":"0000-0001-7048-4627","last_name":"Zhang","first_name":"Xixi","full_name":"Zhang, Xixi"},{"id":"1AE1EA24-02D0-11E9-9BAA-DAF4881429F2","orcid":"0000-0003-0619-7783","last_name":"Glanc","first_name":"Matous","full_name":"Glanc, Matous"},{"last_name":"Li","full_name":"Li, Lanxin","first_name":"Lanxin","orcid":"0000-0002-5607-272X","id":"367EF8FA-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Jaroslav","full_name":"Michalko, Jaroslav","last_name":"Michalko","id":"483727CA-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Pavlovicova, Zlata","first_name":"Zlata","last_name":"Pavlovicova"},{"full_name":"Verstraeten, Inge","first_name":"Inge","last_name":"Verstraeten","id":"362BF7FE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7241-2328"},{"id":"31435098-F248-11E8-B48F-1D18A9856A87","last_name":"Han","full_name":"Han, Huibin","first_name":"Huibin"},{"id":"4800CC20-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2140-7195","last_name":"Hajny","full_name":"Hajny, Jakub","first_name":"Jakub"},{"orcid":"0000-0001-9843-3522","id":"4E01D6B4-F248-11E8-B48F-1D18A9856A87","full_name":"Hauschild, Robert","first_name":"Robert","last_name":"Hauschild"},{"full_name":"Čovanová, Milada","first_name":"Milada","last_name":"Čovanová"},{"last_name":"Zwiewka","full_name":"Zwiewka, Marta","first_name":"Marta"},{"id":"2EEE7A2A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-8295-2926","last_name":"Hörmayer","first_name":"Lukas","full_name":"Hörmayer, Lukas"},{"id":"43905548-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-9767-8699","last_name":"Fendrych","first_name":"Matyas","full_name":"Fendrych, Matyas"},{"last_name":"Xu","full_name":"Xu, Tongda","first_name":"Tongda"},{"full_name":"Vernoux, Teva","first_name":"Teva","last_name":"Vernoux"},{"orcid":"0000-0002-8302-7596","id":"4159519E-F248-11E8-B48F-1D18A9856A87","full_name":"Friml, Jiří","first_name":"Jiří","last_name":"Friml"}],"type":"journal_article","day":"01","title":"Developmental roles of auxin binding protein 1 in Arabidopsis thaliana","ec_funded":1,"citation":{"ama":"Gelová Z, Gallei MC, Pernisová M, et al. Developmental roles of auxin binding protein 1 in Arabidopsis thaliana. <i>Plant Science</i>. 2021;303. doi:<a href=\"https://doi.org/10.1016/j.plantsci.2020.110750\">10.1016/j.plantsci.2020.110750</a>","apa":"Gelová, Z., Gallei, M. C., Pernisová, M., Brunoud, G., Zhang, X., Glanc, M., … Friml, J. (2021). Developmental roles of auxin binding protein 1 in Arabidopsis thaliana. <i>Plant Science</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.plantsci.2020.110750\">https://doi.org/10.1016/j.plantsci.2020.110750</a>","short":"Z. Gelová, M.C. Gallei, M. Pernisová, G. Brunoud, X. Zhang, M. Glanc, L. Li, J. Michalko, Z. Pavlovicova, I. Verstraeten, H. Han, J. Hajny, R. Hauschild, M. Čovanová, M. Zwiewka, L. Hörmayer, M. Fendrych, T. Xu, T. Vernoux, J. Friml, Plant Science 303 (2021).","mla":"Gelová, Zuzana, et al. “Developmental Roles of Auxin Binding Protein 1 in Arabidopsis Thaliana.” <i>Plant Science</i>, vol. 303, 110750, Elsevier, 2021, doi:<a href=\"https://doi.org/10.1016/j.plantsci.2020.110750\">10.1016/j.plantsci.2020.110750</a>.","chicago":"Gelová, Zuzana, Michelle C Gallei, Markéta Pernisová, Géraldine Brunoud, Xixi Zhang, Matous Glanc, Lanxin Li, et al. “Developmental Roles of Auxin Binding Protein 1 in Arabidopsis Thaliana.” <i>Plant Science</i>. Elsevier, 2021. <a href=\"https://doi.org/10.1016/j.plantsci.2020.110750\">https://doi.org/10.1016/j.plantsci.2020.110750</a>.","ieee":"Z. Gelová <i>et al.</i>, “Developmental roles of auxin binding protein 1 in Arabidopsis thaliana,” <i>Plant Science</i>, vol. 303. Elsevier, 2021.","ista":"Gelová Z, Gallei MC, Pernisová M, Brunoud G, Zhang X, Glanc M, Li L, Michalko J, Pavlovicova Z, Verstraeten I, Han H, Hajny J, Hauschild R, Čovanová M, Zwiewka M, Hörmayer L, Fendrych M, Xu T, Vernoux T, Friml J. 2021. Developmental roles of auxin binding protein 1 in Arabidopsis thaliana. Plant Science. 303, 110750."},"volume":303,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"file_date_updated":"2021-02-04T07:49:25Z","oa":1,"publication_status":"published","_id":"8931","abstract":[{"lang":"eng","text":"Auxin is a major plant growth regulator, but current models on auxin perception and signaling cannot explain the whole plethora of auxin effects, in particular those associated with rapid responses. A possible candidate for a component of additional auxin perception mechanisms is the AUXIN BINDING PROTEIN 1 (ABP1), whose function in planta remains unclear.\r\nHere we combined expression analysis with gain- and loss-of-function approaches to analyze the role of ABP1 in plant development. ABP1 shows a broad expression largely overlapping with, but not regulated by, transcriptional auxin response activity. Furthermore, ABP1 activity is not essential for the transcriptional auxin signaling. Genetic in planta analysis revealed that abp1 loss-of-function mutants show largely normal development with minor defects in bolting. On the other hand, ABP1 gain-of-function alleles show a broad range of growth and developmental defects, including root and hypocotyl growth and bending, lateral root and leaf development, bolting, as well as response to heat stress. At the cellular level, ABP1 gain-of-function leads to impaired auxin effect on PIN polar distribution and affects BFA-sensitive PIN intracellular aggregation.\r\nThe gain-of-function analysis suggests a broad, but still mechanistically unclear involvement of ABP1 in plant development, possibly masked in abp1 loss-of-function mutants by a functional redundancy."}],"date_published":"2021-02-01T00:00:00Z","article_number":"110750","file":[{"date_created":"2021-02-04T07:49:25Z","success":1,"file_id":"9083","relation":"main_file","content_type":"application/pdf","checksum":"a7f2562bdca62d67dfa88e271b62a629","access_level":"open_access","date_updated":"2021-02-04T07:49:25Z","creator":"dernst","file_size":12563728,"file_name":"2021_PlantScience_Gelova.pdf"}],"article_processing_charge":"Yes (via OA deal)","acknowledged_ssus":[{"_id":"Bio"},{"_id":"LifeSc"}],"publication_identifier":{"issn":["0168-9452"]},"date_updated":"2024-10-29T10:22:43Z","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","external_id":{"pmid":["33487339"],"isi":["000614154500001"]},"scopus_import":"1","year":"2021","has_accepted_license":"1","oa_version":"Published Version","article_type":"original"},{"year":"2021","oa_version":"Preprint","article_type":"original","publication_identifier":{"issn":["0022-5193"]},"external_id":{"isi":["000659161500002"]},"date_updated":"2023-08-08T13:32:40Z","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","article_processing_charge":"No","_id":"9387","date_published":"2021-04-24T00:00:00Z","abstract":[{"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.","lang":"eng"}],"article_number":"110729","main_file_link":[{"url":"https://www.biorxiv.org/content/10.1101/477489v1","open_access":"1"}],"oa":1,"publication_status":"published","volume":524,"title":"Two linked loci under mutation-selection balance and Muller’s ratchet","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.","ieee":"K. Khudiakova, T. Y. Neretina, and A. S. Kondrashov, “Two linked loci under mutation-selection balance and Muller’s ratchet,” <i>Journal of Theoretical Biology</i>, vol. 524. Elsevier , 2021.","chicago":"Khudiakova, Kseniia, Tatiana Yu. Neretina, and Alexey S. Kondrashov. “Two Linked Loci under Mutation-Selection Balance and Muller’s Ratchet.” <i>Journal of Theoretical Biology</i>. Elsevier , 2021. <a href=\"https://doi.org/10.1016/j.jtbi.2021.110729\">https://doi.org/10.1016/j.jtbi.2021.110729</a>.","mla":"Khudiakova, Kseniia, et al. “Two Linked Loci under Mutation-Selection Balance and Muller’s Ratchet.” <i>Journal of Theoretical Biology</i>, vol. 524, 110729, Elsevier , 2021, doi:<a href=\"https://doi.org/10.1016/j.jtbi.2021.110729\">10.1016/j.jtbi.2021.110729</a>.","short":"K. Khudiakova, T.Y. Neretina, A.S. Kondrashov, Journal of Theoretical Biology 524 (2021).","apa":"Khudiakova, K., Neretina, T. Y., &#38; Kondrashov, A. S. (2021). Two linked loci under mutation-selection balance and Muller’s ratchet. <i>Journal of Theoretical Biology</i>. Elsevier . <a href=\"https://doi.org/10.1016/j.jtbi.2021.110729\">https://doi.org/10.1016/j.jtbi.2021.110729</a>","ama":"Khudiakova K, Neretina TY, Kondrashov AS. Two linked loci under mutation-selection balance and Muller’s ratchet. <i>Journal of Theoretical Biology</i>. 2021;524. doi:<a href=\"https://doi.org/10.1016/j.jtbi.2021.110729\">10.1016/j.jtbi.2021.110729</a>"},"author":[{"last_name":"Khudiakova","first_name":"Kseniia","full_name":"Khudiakova, Kseniia","id":"4E6DC800-AE37-11E9-AC72-31CAE5697425","orcid":"0000-0002-6246-1465"},{"full_name":"Neretina, Tatiana Yu.","first_name":"Tatiana Yu.","last_name":"Neretina"},{"first_name":"Alexey S.","full_name":"Kondrashov, Alexey S.","last_name":"Kondrashov"}],"type":"journal_article","day":"24","acknowledgement":"This work was supported by the Russian Science Foundation grant N 16-14-10173.","doi":"10.1016/j.jtbi.2021.110729","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"],"language":[{"iso":"eng"}],"date_created":"2021-05-12T05:58:42Z","month":"04","isi":1,"publisher":"Elsevier ","status":"public","intvolume":"       524","publication":"Journal of Theoretical Biology","quality_controlled":"1","department":[{"_id":"GradSch"}]},{"article_processing_charge":"No","article_number":"e71575","file":[{"file_id":"10302","relation":"main_file","content_type":"application/pdf","date_created":"2021-11-18T07:02:02Z","success":1,"creator":"lgarciar","file_size":2477302,"file_name":"elife-71575-v1.pdf","checksum":"59318e9e41507cec83c2f4070e6ad540","access_level":"open_access","date_updated":"2021-11-18T07:02:02Z"}],"_id":"10301","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."}],"date_published":"2021-11-17T00:00:00Z","publication_status":"published","oa":1,"file_date_updated":"2021-11-18T07:02:02Z","volume":10,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"article_type":"original","year":"2021","oa_version":"Published Version","has_accepted_license":"1","date_updated":"2023-08-14T11:50:50Z","user_id":"4359f0d1-fa6c-11eb-b949-802e58b17ae8","external_id":{"isi":["000720945900001"]},"publication_identifier":{"issn":["2050-084X"]},"month":"11","date_created":"2021-11-18T06:59:45Z","publisher":"eLife Sciences Publications","isi":1,"quality_controlled":"1","department":[{"_id":"GaNo"}],"publication":"eLife","intvolume":"        10","status":"public","citation":{"ama":"Conde-Dusman MJ, Dey PN, Elía-Zudaire Ó, et al. Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly. <i>eLife</i>. 2021;10. doi:<a href=\"https://doi.org/10.7554/elife.71575\">10.7554/elife.71575</a>","apa":"Conde-Dusman, M. J., Dey, P. N., Elía-Zudaire, Ó., Garcia Rabaneda, L. E., García-Lira, C., Grand, T., … Perez-Otaño, I. (2021). Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.71575\">https://doi.org/10.7554/elife.71575</a>","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).","mla":"Conde-Dusman, María J., et al. “Control of Protein Synthesis and Memory by GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1 Assembly.” <i>ELife</i>, vol. 10, e71575, eLife Sciences Publications, 2021, doi:<a href=\"https://doi.org/10.7554/elife.71575\">10.7554/elife.71575</a>.","chicago":"Conde-Dusman, María J, Partha N Dey, Óscar Elía-Zudaire, Luis E Garcia Rabaneda, Carmen García-Lira, Teddy Grand, Victor Briz, et al. “Control of Protein Synthesis and Memory by GluN3A-NMDA Receptors through Inhibition of GIT1/MTORC1 Assembly.” <i>ELife</i>. eLife Sciences Publications, 2021. <a href=\"https://doi.org/10.7554/elife.71575\">https://doi.org/10.7554/elife.71575</a>.","ieee":"M. J. Conde-Dusman <i>et al.</i>, “Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly,” <i>eLife</i>, vol. 10. eLife Sciences Publications, 2021.","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."},"title":"Control of protein synthesis and memory by GluN3A-NMDA receptors through inhibition of GIT1/mTORC1 assembly","day":"17","type":"journal_article","author":[{"full_name":"Conde-Dusman, María J","first_name":"María J","last_name":"Conde-Dusman"},{"last_name":"Dey","first_name":"Partha N","full_name":"Dey, Partha N"},{"first_name":"Óscar","full_name":"Elía-Zudaire, Óscar","last_name":"Elía-Zudaire"},{"id":"33D1B084-F248-11E8-B48F-1D18A9856A87","first_name":"Luis E","full_name":"Garcia Rabaneda, Luis E","last_name":"Garcia Rabaneda"},{"last_name":"García-Lira","first_name":"Carmen","full_name":"García-Lira, Carmen"},{"first_name":"Teddy","full_name":"Grand, Teddy","last_name":"Grand"},{"first_name":"Victor","full_name":"Briz, Victor","last_name":"Briz"},{"first_name":"Eric R","full_name":"Velasco, Eric R","last_name":"Velasco"},{"first_name":"Raül","full_name":"Andero Galí, Raül","last_name":"Andero Galí"},{"last_name":"Niñerola","full_name":"Niñerola, Sergio","first_name":"Sergio"},{"full_name":"Barco, Angel","first_name":"Angel","last_name":"Barco"},{"first_name":"Pierre","full_name":"Paoletti, Pierre","last_name":"Paoletti"},{"first_name":"John F","full_name":"Wesseling, John F","last_name":"Wesseling"},{"full_name":"Gardoni, Fabrizio","first_name":"Fabrizio","last_name":"Gardoni"},{"last_name":"Tavalin","full_name":"Tavalin, Steven J","first_name":"Steven J"},{"last_name":"Perez-Otaño","first_name":"Isabel","full_name":"Perez-Otaño, Isabel"}],"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).","language":[{"iso":"eng"}],"keyword":["general immunology and microbiology","general biochemistry","genetics and molecular biology","general medicine","general neuroscience"],"ddc":["570"],"doi":"10.7554/elife.71575"},{"publisher":"eLife Sciences Publications","quality_controlled":"1","publication":"eLife","status":"public","intvolume":"         9","extern":"1","month":"09","date_created":"2022-04-07T07:43:48Z","pmid":1,"language":[{"iso":"eng"}],"keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"ddc":["570"],"doi":"10.7554/elife.54383","citation":{"short":"S. Bersini, R. Schulte, L. Huang, H. Tsai, M. Hetzer, ELife 9 (2020).","ama":"Bersini S, Schulte R, Huang L, Tsai H, Hetzer M. Direct reprogramming of human smooth muscle and vascular endothelial cells reveals defects associated with aging and Hutchinson-Gilford progeria syndrome. <i>eLife</i>. 2020;9. doi:<a href=\"https://doi.org/10.7554/elife.54383\">10.7554/elife.54383</a>","apa":"Bersini, S., Schulte, R., Huang, L., Tsai, H., &#38; Hetzer, M. (2020). Direct reprogramming of human smooth muscle and vascular endothelial cells reveals defects associated with aging and Hutchinson-Gilford progeria syndrome. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.54383\">https://doi.org/10.7554/elife.54383</a>","chicago":"Bersini, Simone, Roberta Schulte, Ling Huang, Hannah Tsai, and Martin Hetzer. “Direct Reprogramming of Human Smooth Muscle and Vascular Endothelial Cells Reveals Defects Associated with Aging and Hutchinson-Gilford Progeria Syndrome.” <i>ELife</i>. eLife Sciences Publications, 2020. <a href=\"https://doi.org/10.7554/elife.54383\">https://doi.org/10.7554/elife.54383</a>.","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.","ieee":"S. Bersini, R. Schulte, L. Huang, H. Tsai, and M. Hetzer, “Direct reprogramming of human smooth muscle and vascular endothelial cells reveals defects associated with aging and Hutchinson-Gilford progeria syndrome,” <i>eLife</i>, vol. 9. eLife Sciences Publications, 2020.","mla":"Bersini, Simone, et al. “Direct Reprogramming of Human Smooth Muscle and Vascular Endothelial Cells Reveals Defects Associated with Aging and Hutchinson-Gilford Progeria Syndrome.” <i>ELife</i>, vol. 9, e54383, eLife Sciences Publications, 2020, doi:<a href=\"https://doi.org/10.7554/elife.54383\">10.7554/elife.54383</a>."},"title":"Direct reprogramming of human smooth muscle and vascular endothelial cells reveals defects associated with aging and Hutchinson-Gilford progeria syndrome","day":"08","type":"journal_article","author":[{"last_name":"Bersini","full_name":"Bersini, Simone","first_name":"Simone"},{"first_name":"Roberta","full_name":"Schulte, Roberta","last_name":"Schulte"},{"last_name":"Huang","first_name":"Ling","full_name":"Huang, Ling"},{"last_name":"Tsai","first_name":"Hannah","full_name":"Tsai, Hannah"},{"last_name":"HETZER","full_name":"HETZER, Martin W","first_name":"Martin W","orcid":"0000-0002-2111-992X","id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed"}],"publication_status":"published","oa":1,"file_date_updated":"2022-04-08T06:53:10Z","volume":9,"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"article_processing_charge":"No","article_number":"e54383","file":[{"content_type":"application/pdf","file_id":"11132","relation":"main_file","date_created":"2022-04-08T06:53:10Z","success":1,"file_name":"2020_eLife_Bersini.pdf","creator":"dernst","file_size":4399825,"checksum":"f8b3821349a194050be02570d8fe7d4b","date_updated":"2022-04-08T06:53:10Z","access_level":"open_access"}],"_id":"11055","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"}],"date_published":"2020-09-08T00:00:00Z","user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","date_updated":"2022-07-18T08:30:37Z","external_id":{"pmid":["32896271"]},"scopus_import":"1","publication_identifier":{"issn":["2050-084X"]},"article_type":"original","has_accepted_license":"1","year":"2020","oa_version":"Published Version"},{"author":[{"last_name":"Brázdil","first_name":"Tomáš","full_name":"Brázdil, Tomáš"},{"last_name":"Chatterjee","first_name":"Krishnendu","full_name":"Chatterjee, Krishnendu","orcid":"0000-0002-4561-241X","id":"2E5DCA20-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Novotný","full_name":"Novotný, Petr","first_name":"Petr"},{"first_name":"Jiří","full_name":"Vahala, Jiří","last_name":"Vahala"}],"type":"journal_article","day":"03","title":"Reinforcement learning of risk-constrained policies in Markov decision processes","conference":{"location":"New York, NY, United States","end_date":"2020-02-12","start_date":"2020-02-07","name":"AAAI: Conference on Artificial Intelligence"},"citation":{"ama":"Brázdil T, Chatterjee K, Novotný P, Vahala J. Reinforcement learning of risk-constrained policies in Markov decision processes. <i>Proceedings of the 34th AAAI Conference on Artificial Intelligence</i>. 2020;34(06):9794-9801. doi:<a href=\"https://doi.org/10.1609/aaai.v34i06.6531\">10.1609/aaai.v34i06.6531</a>","apa":"Brázdil, T., Chatterjee, K., Novotný, P., &#38; Vahala, J. (2020). Reinforcement learning of risk-constrained policies in Markov decision processes. <i>Proceedings of the 34th AAAI Conference on Artificial Intelligence</i>. New York, NY, United States: Association for the Advancement of Artificial Intelligence. <a href=\"https://doi.org/10.1609/aaai.v34i06.6531\">https://doi.org/10.1609/aaai.v34i06.6531</a>","short":"T. Brázdil, K. Chatterjee, P. Novotný, J. Vahala, Proceedings of the 34th AAAI Conference on Artificial Intelligence 34 (2020) 9794–9801.","mla":"Brázdil, Tomáš, et al. “Reinforcement Learning of Risk-Constrained Policies in Markov Decision Processes.” <i>Proceedings of the 34th AAAI Conference on Artificial Intelligence</i>, vol. 34, no. 06, Association for the Advancement of Artificial Intelligence, 2020, pp. 9794–801, doi:<a href=\"https://doi.org/10.1609/aaai.v34i06.6531\">10.1609/aaai.v34i06.6531</a>.","chicago":"Brázdil, Tomáš, Krishnendu Chatterjee, Petr Novotný, and Jiří Vahala. “Reinforcement Learning of Risk-Constrained Policies in Markov Decision Processes.” <i>Proceedings of the 34th AAAI Conference on Artificial Intelligence</i>. Association for the Advancement of Artificial Intelligence, 2020. <a href=\"https://doi.org/10.1609/aaai.v34i06.6531\">https://doi.org/10.1609/aaai.v34i06.6531</a>.","ista":"Brázdil T, Chatterjee K, Novotný P, Vahala J. 2020. Reinforcement learning of risk-constrained policies in Markov decision processes. Proceedings of the 34th AAAI Conference on Artificial Intelligence. 34(06), 9794–9801.","ieee":"T. Brázdil, K. Chatterjee, P. Novotný, and J. Vahala, “Reinforcement learning of risk-constrained policies in Markov decision processes,” <i>Proceedings of the 34th AAAI Conference on Artificial Intelligence</i>, vol. 34, no. 06. Association for the Advancement of Artificial Intelligence, pp. 9794–9801, 2020."},"doi":"10.1609/aaai.v34i06.6531","keyword":["General Medicine"],"language":[{"iso":"eng"}],"project":[{"name":"Game Theory","grant_number":"S11407","_id":"25863FF4-B435-11E9-9278-68D0E5697425","call_identifier":"FWF"}],"acknowledgement":"Krishnendu Chatterjee is supported by the Austrian Science Fund (FWF) NFN Grant No. S11407-N23 (RiSE/SHiNE), and COST Action GAMENET. Tomas Brazdil is supported by the Grant Agency of Masaryk University grant no. MUNI/G/0739/2017 and by the Czech Science Foundation grant No. 18-11193S. Petr Novotny and Jirı Vahala are supported by the Czech Science Foundation grant No. GJ19-15134Y.","date_created":"2024-03-04T08:07:22Z","month":"04","page":"9794-9801","status":"public","intvolume":"        34","publication":"Proceedings of the 34th AAAI Conference on Artificial Intelligence","quality_controlled":"1","department":[{"_id":"KrCh"}],"publisher":"Association for the Advancement of Artificial Intelligence","year":"2020","oa_version":"Preprint","article_type":"original","publication_identifier":{"issn":["2374-3468"]},"external_id":{"arxiv":["2002.12086"]},"date_updated":"2024-03-04T08:30:16Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_published":"2020-04-03T00:00:00Z","_id":"15055","abstract":[{"lang":"eng","text":"<jats:p>Markov decision processes (MDPs) are the defacto framework for sequential decision making in the presence of stochastic uncertainty. A classical optimization criterion for MDPs is to maximize the expected discounted-sum payoff, which ignores low probability catastrophic events with highly negative impact on the system. On the other hand, risk-averse policies require the probability of undesirable events to be below a given threshold, but they do not account for optimization of the expected payoff. We consider MDPs with discounted-sum payoff with failure states which represent catastrophic outcomes. The objective of risk-constrained planning is to maximize the expected discounted-sum payoff among risk-averse policies that ensure the probability to encounter a failure state is below a desired threshold. Our main contribution is an efficient risk-constrained planning algorithm that combines UCT-like search with a predictor learned through interaction with the MDP (in the style of AlphaZero) and with a risk-constrained action selection via linear programming. We demonstrate the effectiveness of our approach with experiments on classical MDPs from the literature, including benchmarks with an order of 106 states.</jats:p>"}],"article_processing_charge":"No","issue":"06","arxiv":1,"volume":34,"oa":1,"main_file_link":[{"open_access":"1","url":"https://doi.org/10.48550/arXiv.2002.12086"}],"publication_status":"published"},{"status":"public","intvolume":"         1","quality_controlled":"1","department":[{"_id":"LaEr"}],"publication":"Probability and Mathematical Physics","publisher":"Mathematical Sciences Publishers","date_created":"2024-03-04T10:27:57Z","month":"11","page":"101-146","doi":"10.2140/pmp.2020.1.101","language":[{"iso":"eng"}],"keyword":["General Medicine"],"acknowledgement":"Partially supported by ERC Advanced Grant No. 338804. This project has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie Grant Agreement No. 66538","project":[{"call_identifier":"FP7","_id":"258DCDE6-B435-11E9-9278-68D0E5697425","name":"Random matrices, universality and disordered quantum systems","grant_number":"338804"},{"call_identifier":"H2020","_id":"2564DBCA-B435-11E9-9278-68D0E5697425","name":"International IST Doctoral Program","grant_number":"665385"}],"type":"journal_article","author":[{"last_name":"Cipolloni","full_name":"Cipolloni, Giorgio","first_name":"Giorgio","id":"42198EFA-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-4901-7992"},{"id":"4DBD5372-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5366-9603","first_name":"László","full_name":"Erdös, László","last_name":"Erdös"},{"id":"408ED176-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-2904-1856","first_name":"Dominik J","full_name":"Schröder, Dominik J","last_name":"Schröder"}],"day":"16","title":"Optimal lower bound on the least singular value of the shifted Ginibre ensemble","ec_funded":1,"citation":{"ama":"Cipolloni G, Erdös L, Schröder DJ. Optimal lower bound on the least singular value of the shifted Ginibre ensemble. <i>Probability and Mathematical Physics</i>. 2020;1(1):101-146. doi:<a href=\"https://doi.org/10.2140/pmp.2020.1.101\">10.2140/pmp.2020.1.101</a>","apa":"Cipolloni, G., Erdös, L., &#38; Schröder, D. J. (2020). Optimal lower bound on the least singular value of the shifted Ginibre ensemble. <i>Probability and Mathematical Physics</i>. Mathematical Sciences Publishers. <a href=\"https://doi.org/10.2140/pmp.2020.1.101\">https://doi.org/10.2140/pmp.2020.1.101</a>","short":"G. Cipolloni, L. Erdös, D.J. Schröder, Probability and Mathematical Physics 1 (2020) 101–146.","mla":"Cipolloni, Giorgio, et al. “Optimal Lower Bound on the Least Singular Value of the Shifted Ginibre Ensemble.” <i>Probability and Mathematical Physics</i>, vol. 1, no. 1, Mathematical Sciences Publishers, 2020, pp. 101–46, doi:<a href=\"https://doi.org/10.2140/pmp.2020.1.101\">10.2140/pmp.2020.1.101</a>.","chicago":"Cipolloni, Giorgio, László Erdös, and Dominik J Schröder. “Optimal Lower Bound on the Least Singular Value of the Shifted Ginibre Ensemble.” <i>Probability and Mathematical Physics</i>. Mathematical Sciences Publishers, 2020. <a href=\"https://doi.org/10.2140/pmp.2020.1.101\">https://doi.org/10.2140/pmp.2020.1.101</a>.","ista":"Cipolloni G, Erdös L, Schröder DJ. 2020. Optimal lower bound on the least singular value of the shifted Ginibre ensemble. Probability and Mathematical Physics. 1(1), 101–146.","ieee":"G. Cipolloni, L. Erdös, and D. J. Schröder, “Optimal lower bound on the least singular value of the shifted Ginibre ensemble,” <i>Probability and Mathematical Physics</i>, vol. 1, no. 1. Mathematical Sciences Publishers, pp. 101–146, 2020."},"volume":1,"main_file_link":[{"open_access":"1","url":"https://doi.org/10.48550/arXiv.1908.01653"}],"oa":1,"publication_status":"published","_id":"15063","date_published":"2020-11-16T00:00:00Z","abstract":[{"lang":"eng","text":"We consider the least singular value of a large random matrix with real or complex i.i.d. Gaussian entries shifted by a constant z∈C. We prove an optimal lower tail estimate on this singular value in the critical regime where z is around the spectral edge, thus improving the classical bound of Sankar, Spielman and Teng (SIAM J. Matrix Anal. Appl. 28:2 (2006), 446–476) for the particular shift-perturbation in the edge regime. Lacking Brézin–Hikami formulas in the real case, we rely on the superbosonization formula (Comm. Math. Phys. 283:2 (2008), 343–395)."}],"issue":"1","article_processing_charge":"No","arxiv":1,"publication_identifier":{"issn":["2690-1005","2690-0998"]},"date_updated":"2024-03-04T10:33:15Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","external_id":{"arxiv":["1908.01653"]},"scopus_import":"1","year":"2020","oa_version":"Preprint","article_type":"original"},{"main_file_link":[{"open_access":"1","url":"https://doi.org/10.1021/acs.accounts.0c00434"}],"oa":1,"publication_status":"published","volume":53,"article_processing_charge":"No","issue":"11","_id":"13361","abstract":[{"text":"In nature, light is harvested by photoactive proteins to drive a range of biological processes, including photosynthesis, phototaxis, vision, and ultimately life. Bacteriorhodopsin, for example, is a protein embedded within archaeal cell membranes that binds the chromophore retinal within its hydrophobic pocket. Exposure to light triggers regioselective photoisomerization of the confined retinal, which in turn initiates a cascade of conformational changes within the protein, triggering proton flux against the concentration gradient, providing the microorganisms with the energy to live. We are inspired by these functions in nature to harness light energy using synthetic photoswitches under confinement. Like retinal, synthetic photoswitches require some degree of conformational flexibility to isomerize. In nature, the conformational change associated with retinal isomerization is accommodated by the structural flexibility of the opsin host, yet it results in steric communication between the chromophore and the protein. Similarly, we strive to design systems wherein isomerization of confined photoswitches results in steric communication between a photoswitch and its confining environment. To achieve this aim, a balance must be struck between molecular crowding and conformational freedom under confinement: too much crowding prevents switching, whereas too much freedom resembles switching of isolated molecules in solution, preventing communication.\r\n\r\nIn this Account, we discuss five classes of synthetic light-switchable compounds—diarylethenes, anthracenes, azobenzenes, spiropyrans, and donor–acceptor Stenhouse adducts—comparing their behaviors under confinement and in solution. The environments employed to confine these photoswitches are diverse, ranging from planar surfaces to nanosized cavities within coordination cages, nanoporous frameworks, and nanoparticle aggregates. The trends that emerge are primarily dependent on the nature of the photoswitch and not on the material used for confinement. In general, we find that photoswitches requiring less conformational freedom for switching are, as expected, more straightforward to isomerize reversibly under confinement. Because these compounds undergo only small structural changes upon isomerization, however, switching does not propagate into communication with their environment. Conversely, photoswitches that require more conformational freedom are more challenging to switch under confinement but also can influence system-wide behavior.\r\n\r\nAlthough we are primarily interested in the effects of geometric constraints on photoswitching under confinement, additional effects inevitably emerge when a compound is removed from solution and placed within a new, more crowded environment. For instance, we have found that compounds that convert to zwitterionic isomers upon light irradiation often experience stabilization of these forms under confinement. This effect results from the mutual stabilization of zwitterions that are brought into close proximity on surfaces or within cavities. Furthermore, photoswitches can experience preorganization under confinement, influencing the selectivity and efficiency of their photoreactions. Because intermolecular interactions arising from confinement cannot be considered independently from the effects of geometric constraints, we describe all confinement effects concurrently throughout this Account.","lang":"eng"}],"date_published":"2020-11-17T00:00:00Z","publication_identifier":{"eissn":["1520-4898"],"issn":["0001-4842"]},"external_id":{"pmid":["32969638"]},"scopus_import":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2023-08-07T10:06:46Z","oa_version":"Published Version","year":"2020","article_type":"original","publisher":"American Chemical Society","intvolume":"        53","status":"public","publication":"Accounts of Chemical Research","quality_controlled":"1","page":"2600-2610","date_created":"2023-08-01T09:35:50Z","month":"11","extern":"1","pmid":1,"doi":"10.1021/acs.accounts.0c00434","keyword":["General Medicine","General Chemistry"],"language":[{"iso":"eng"}],"title":"Molecular photoswitching in confined spaces","citation":{"mla":"Grommet, Angela B., et al. “Molecular Photoswitching in Confined Spaces.” <i>Accounts of Chemical Research</i>, vol. 53, no. 11, American Chemical Society, 2020, pp. 2600–10, doi:<a href=\"https://doi.org/10.1021/acs.accounts.0c00434\">10.1021/acs.accounts.0c00434</a>.","chicago":"Grommet, Angela B., Lucia M. Lee, and Rafal Klajn. “Molecular Photoswitching in Confined Spaces.” <i>Accounts of Chemical Research</i>. American Chemical Society, 2020. <a href=\"https://doi.org/10.1021/acs.accounts.0c00434\">https://doi.org/10.1021/acs.accounts.0c00434</a>.","ista":"Grommet AB, Lee LM, Klajn R. 2020. Molecular photoswitching in confined spaces. Accounts of Chemical Research. 53(11), 2600–2610.","ieee":"A. B. Grommet, L. M. Lee, and R. Klajn, “Molecular photoswitching in confined spaces,” <i>Accounts of Chemical Research</i>, vol. 53, no. 11. American Chemical Society, pp. 2600–2610, 2020.","ama":"Grommet AB, Lee LM, Klajn R. Molecular photoswitching in confined spaces. <i>Accounts of Chemical Research</i>. 2020;53(11):2600-2610. doi:<a href=\"https://doi.org/10.1021/acs.accounts.0c00434\">10.1021/acs.accounts.0c00434</a>","apa":"Grommet, A. B., Lee, L. M., &#38; Klajn, R. (2020). Molecular photoswitching in confined spaces. <i>Accounts of Chemical Research</i>. American Chemical Society. <a href=\"https://doi.org/10.1021/acs.accounts.0c00434\">https://doi.org/10.1021/acs.accounts.0c00434</a>","short":"A.B. Grommet, L.M. Lee, R. Klajn, Accounts of Chemical Research 53 (2020) 2600–2610."},"author":[{"last_name":"Grommet","first_name":"Angela B.","full_name":"Grommet, Angela B."},{"last_name":"Lee","first_name":"Lucia M.","full_name":"Lee, Lucia M."},{"id":"8e84690e-1e48-11ed-a02b-a1e6fb8bb53b","last_name":"Klajn","full_name":"Klajn, Rafal","first_name":"Rafal"}],"type":"journal_article","day":"17"},{"article_type":"original","oa_version":"Published Version","year":"2019","has_accepted_license":"1","scopus_import":"1","external_id":{"pmid":["31599721"]},"user_id":"72615eeb-f1f3-11ec-aa25-d4573ddc34fd","date_updated":"2023-05-31T06:36:22Z","publication_identifier":{"issn":["2050-084X"]},"article_number":"e49796","file":[{"success":1,"date_created":"2022-04-08T08:18:01Z","content_type":"application/pdf","relation":"main_file","file_id":"11138","date_updated":"2022-04-08T08:18:01Z","access_level":"open_access","checksum":"1e8672a1e9c3dc0a2d3d0dad89673616","file_name":"2019_eLife_Buchwalter.pdf","file_size":6984654,"creator":"dernst"}],"_id":"11060","date_published":"2019-10-10T00:00:00Z","abstract":[{"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.","lang":"eng"}],"article_processing_charge":"No","file_date_updated":"2022-04-08T08:18:01Z","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"volume":8,"publication_status":"published","oa":1,"day":"10","type":"journal_article","author":[{"full_name":"Buchwalter, Abigail","first_name":"Abigail","last_name":"Buchwalter"},{"first_name":"Roberta","full_name":"Schulte, Roberta","last_name":"Schulte"},{"first_name":"Hsiao","full_name":"Tsai, Hsiao","last_name":"Tsai"},{"full_name":"Capitanio, Juliana","first_name":"Juliana","last_name":"Capitanio"},{"id":"86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed","orcid":"0000-0002-2111-992X","last_name":"HETZER","first_name":"Martin W","full_name":"HETZER, Martin W"}],"citation":{"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.","ieee":"A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, and M. Hetzer, “Selective clearance of the inner nuclear membrane protein emerin by vesicular transport during ER stress,” <i>eLife</i>, vol. 8. eLife Sciences Publications, 2019.","chicago":"Buchwalter, Abigail, Roberta Schulte, Hsiao Tsai, Juliana Capitanio, and Martin Hetzer. “Selective Clearance of the Inner Nuclear Membrane Protein Emerin by Vesicular Transport during ER Stress.” <i>ELife</i>. eLife Sciences Publications, 2019. <a href=\"https://doi.org/10.7554/elife.49796\">https://doi.org/10.7554/elife.49796</a>.","mla":"Buchwalter, Abigail, et al. “Selective Clearance of the Inner Nuclear Membrane Protein Emerin by Vesicular Transport during ER Stress.” <i>ELife</i>, vol. 8, e49796, eLife Sciences Publications, 2019, doi:<a href=\"https://doi.org/10.7554/elife.49796\">10.7554/elife.49796</a>.","short":"A. Buchwalter, R. Schulte, H. Tsai, J. Capitanio, M. Hetzer, ELife 8 (2019).","apa":"Buchwalter, A., Schulte, R., Tsai, H., Capitanio, J., &#38; Hetzer, M. (2019). Selective clearance of the inner nuclear membrane protein emerin by vesicular transport during ER stress. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.49796\">https://doi.org/10.7554/elife.49796</a>","ama":"Buchwalter A, Schulte R, Tsai H, Capitanio J, Hetzer M. Selective clearance of the inner nuclear membrane protein emerin by vesicular transport during ER stress. <i>eLife</i>. 2019;8. doi:<a href=\"https://doi.org/10.7554/elife.49796\">10.7554/elife.49796</a>"},"title":"Selective clearance of the inner nuclear membrane protein emerin by vesicular transport during ER stress","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"language":[{"iso":"eng"}],"ddc":["570"],"doi":"10.7554/elife.49796","pmid":1,"related_material":{"record":[{"status":"public","relation":"research_data","id":"13079"}]},"month":"10","extern":"1","date_created":"2022-04-07T07:45:02Z","publication":"eLife","quality_controlled":"1","status":"public","intvolume":"         8","publisher":"eLife Sciences Publications"},{"article_type":"original","oa_version":"Published Version","year":"2019","has_accepted_license":"1","external_id":{"unknown":["31135340"]},"scopus_import":"1","date_updated":"2023-05-08T10:54:12Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication_identifier":{"issn":["2050-084X"]},"article_processing_charge":"No","article_number":"42530","file":[{"checksum":"ea6b89c20d59e5eb3646916fe5d568ad","date_updated":"2023-02-07T09:42:46Z","access_level":"open_access","file_name":"2019_elife_He.pdf","creator":"alisjak","file_size":2493837,"date_created":"2023-02-07T09:42:46Z","success":1,"content_type":"application/pdf","file_id":"12525","relation":"main_file"}],"_id":"12192","abstract":[{"lang":"eng","text":"Transposable elements (TEs), the movement of which can damage the genome, are epigenetically silenced in eukaryotes. Intriguingly, TEs are activated in the sperm companion cell – vegetative cell (VC) – of the flowering plant Arabidopsis thaliana. However, the extent and mechanism of this activation are unknown. Here we show that about 100 heterochromatic TEs are activated in VCs, mostly by DEMETER-catalyzed DNA demethylation. We further demonstrate that DEMETER access to some of these TEs is permitted by the natural depletion of linker histone H1 in VCs. Ectopically expressed H1 suppresses TEs in VCs by reducing DNA demethylation and via a methylation-independent mechanism. We demonstrate that H1 is required for heterochromatin condensation in plant cells and show that H1 overexpression creates heterochromatic foci in the VC progenitor cell. Taken together, our results demonstrate that the natural depletion of H1 during male gametogenesis facilitates DEMETER-directed DNA demethylation, heterochromatin relaxation, and TE activation."}],"date_published":"2019-05-28T00:00:00Z","publication_status":"published","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6594752/","open_access":"1"}],"oa":1,"file_date_updated":"2023-02-07T09:42:46Z","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"volume":8,"citation":{"short":"S. He, M. Vickers, J. Zhang, X. Feng, ELife 8 (2019).","ama":"He S, Vickers M, Zhang J, Feng X. Natural depletion of histone H1 in sex cells causes DNA demethylation, heterochromatin decondensation and transposon activation. <i>eLife</i>. 2019;8. doi:<a href=\"https://doi.org/10.7554/elife.42530\">10.7554/elife.42530</a>","apa":"He, S., Vickers, M., Zhang, J., &#38; Feng, X. (2019). Natural depletion of histone H1 in sex cells causes DNA demethylation, heterochromatin decondensation and transposon activation. <i>ELife</i>. eLife Sciences Publications, Ltd. <a href=\"https://doi.org/10.7554/elife.42530\">https://doi.org/10.7554/elife.42530</a>","chicago":"He, Shengbo, Martin Vickers, Jingyi Zhang, and Xiaoqi Feng. “Natural Depletion of Histone H1 in Sex Cells Causes DNA Demethylation, Heterochromatin Decondensation and Transposon Activation.” <i>ELife</i>. eLife Sciences Publications, Ltd, 2019. <a href=\"https://doi.org/10.7554/elife.42530\">https://doi.org/10.7554/elife.42530</a>.","ista":"He S, Vickers M, Zhang J, Feng X. 2019. Natural depletion of histone H1 in sex cells causes DNA demethylation, heterochromatin decondensation and transposon activation. eLife. 8, 42530.","ieee":"S. He, M. Vickers, J. Zhang, and X. Feng, “Natural depletion of histone H1 in sex cells causes DNA demethylation, heterochromatin decondensation and transposon activation,” <i>eLife</i>, vol. 8. eLife Sciences Publications, Ltd, 2019.","mla":"He, Shengbo, et al. “Natural Depletion of Histone H1 in Sex Cells Causes DNA Demethylation, Heterochromatin Decondensation and Transposon Activation.” <i>ELife</i>, vol. 8, 42530, eLife Sciences Publications, Ltd, 2019, doi:<a href=\"https://doi.org/10.7554/elife.42530\">10.7554/elife.42530</a>."},"title":"Natural depletion of histone H1 in sex cells causes DNA demethylation, heterochromatin decondensation and transposon activation","day":"28","author":[{"last_name":"He","first_name":"Shengbo","full_name":"He, Shengbo"},{"last_name":"Vickers","first_name":"Martin","full_name":"Vickers, Martin"},{"first_name":"Jingyi","full_name":"Zhang, Jingyi","last_name":"Zhang"},{"last_name":"Feng","first_name":"Xiaoqi","full_name":"Feng, Xiaoqi","orcid":"0000-0002-4008-1234","id":"e0164712-22ee-11ed-b12a-d80fcdf35958"}],"type":"journal_article","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).","keyword":["General Immunology and Microbiology","General Biochemistry","Genetics and Molecular Biology","General Medicine","General Neuroscience"],"language":[{"iso":"eng"}],"doi":"10.7554/elife.42530","ddc":["580"],"month":"05","extern":"1","date_created":"2023-01-16T09:17:21Z","publisher":"eLife Sciences Publications, Ltd","publication":"eLife","department":[{"_id":"XiFe"}],"quality_controlled":"1","intvolume":"         8","status":"public"},{"article_processing_charge":"No","issue":"5","_id":"10880","abstract":[{"lang":"eng","text":"Acquisition of evolutionary novelties is a fundamental process for adapting to the external environment and invading new niches and results in the diversification of life, which we can see in the world today. How such novel phenotypic traits are acquired in the course of evolution and are built up in developing embryos has been a central question in biology. Whole-genome duplication (WGD) is a process of genome doubling that supplies raw genetic materials and increases genome complexity. Recently, it has been gradually revealed that WGD and subsequent fate changes of duplicated genes can facilitate phenotypic evolution. Here, we review the current understanding of the relationship between WGD and the acquisition of evolutionary novelties. We show some examples of this link and discuss how WGD and subsequent duplicated genes can facilitate phenotypic evolution as well as when such genomic doubling can be advantageous for adaptation."}],"date_published":"2018-09-01T00:00:00Z","main_file_link":[{"url":"https://doi.org/10.1093/bfgp/ely007","open_access":"1"}],"oa":1,"publication_status":"published","volume":17,"year":"2018","oa_version":"Published Version","article_type":"original","publication_identifier":{"issn":["2041-2649"],"eissn":["2041-2657"]},"scopus_import":"1","external_id":{"pmid":["29579140"],"isi":["000456054400004"]},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","date_updated":"2023-09-19T15:11:22Z","page":"329-338","date_created":"2022-03-18T12:40:35Z","month":"09","isi":1,"publisher":"Oxford University Press","intvolume":"        17","status":"public","publication":"Briefings in Functional Genomics","quality_controlled":"1","department":[{"_id":"CaHe"}],"title":"Significance of whole-genome duplications on the emergence of evolutionary novelties","citation":{"chicago":"Yuuta, Moriyama, and Kazuko Koshiba-Takeuchi. “Significance of Whole-Genome Duplications on the Emergence of Evolutionary Novelties.” <i>Briefings in Functional Genomics</i>. Oxford University Press, 2018. <a href=\"https://doi.org/10.1093/bfgp/ely007\">https://doi.org/10.1093/bfgp/ely007</a>.","ista":"Yuuta M, Koshiba-Takeuchi K. 2018. Significance of whole-genome duplications on the emergence of evolutionary novelties. Briefings in Functional Genomics. 17(5), 329–338.","ieee":"M. Yuuta and K. Koshiba-Takeuchi, “Significance of whole-genome duplications on the emergence of evolutionary novelties,” <i>Briefings in Functional Genomics</i>, vol. 17, no. 5. Oxford University Press, pp. 329–338, 2018.","mla":"Yuuta, Moriyama, and Kazuko Koshiba-Takeuchi. “Significance of Whole-Genome Duplications on the Emergence of Evolutionary Novelties.” <i>Briefings in Functional Genomics</i>, vol. 17, no. 5, Oxford University Press, 2018, pp. 329–38, doi:<a href=\"https://doi.org/10.1093/bfgp/ely007\">10.1093/bfgp/ely007</a>.","short":"M. Yuuta, K. Koshiba-Takeuchi, Briefings in Functional Genomics 17 (2018) 329–338.","ama":"Yuuta M, Koshiba-Takeuchi K. Significance of whole-genome duplications on the emergence of evolutionary novelties. <i>Briefings in Functional Genomics</i>. 2018;17(5):329-338. doi:<a href=\"https://doi.org/10.1093/bfgp/ely007\">10.1093/bfgp/ely007</a>","apa":"Yuuta, M., &#38; Koshiba-Takeuchi, K. (2018). Significance of whole-genome duplications on the emergence of evolutionary novelties. <i>Briefings in Functional Genomics</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/bfgp/ely007\">https://doi.org/10.1093/bfgp/ely007</a>"},"type":"journal_article","author":[{"last_name":"Yuuta","first_name":"Moriyama","full_name":"Yuuta, Moriyama","orcid":"0000-0002-2853-8051","id":"4968E7C8-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Koshiba-Takeuchi","first_name":"Kazuko","full_name":"Koshiba-Takeuchi, Kazuko"}],"day":"01","pmid":1,"acknowledgement":"This work was supported by JSPS overseas research fellowships (Y.M.) and SENSHIN Medical Research Foundation (K.K.T.).","doi":"10.1093/bfgp/ely007","keyword":["Genetics","Molecular Biology","Biochemistry","General Medicine"],"language":[{"iso":"eng"}]},{"publication_status":"published","publisher":"American Chemical Society","volume":13,"intvolume":"        13","status":"public","quality_controlled":"1","publication":"ACS Chemical Biology","issue":"8","article_processing_charge":"No","page":"2106-2113","abstract":[{"text":"Lipopolysaccharides (LPS) are complex glycolipids forming the outside layer of Gram-negative bacteria. Their hydrophobic and heterogeneous nature greatly hampers their structural study in an environment similar to the bacterial surface. We have studied LPS purified from E. coli and pathogenic P. aeruginosa with long O-antigen polysaccharides assembled in solution as vesicles or elongated micelles. Solid-state NMR with magic-angle spinning permitted the identification of NMR signals arising from regions with different flexibilities in the LPS, from the lipid components to the O-antigen polysaccharides. Atomic scale data on the LPS enabled the study of the interaction of gentamicin antibiotic bound to P. aeruginosa LPS, for which we could confirm that a specific oligosaccharide is involved in the antibiotic binding. The possibility to study LPS alone and bound to a ligand when it is assembled in membrane-like structures opens great prospects for the investigation of proteins and antibiotics that specifically target such an important molecule at the surface of Gram-negative bacteria.","lang":"eng"}],"_id":"8439","date_published":"2018-07-02T00:00:00Z","date_created":"2020-09-18T10:05:09Z","extern":"1","month":"07","doi":"10.1021/acschembio.8b00271","publication_identifier":{"issn":["1554-8929","1554-8937"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2021-01-12T08:19:16Z","language":[{"iso":"eng"}],"keyword":["Molecular Medicine","Biochemistry","General Medicine"],"title":"Solid state NMR studies of intact lipopolysaccharide endotoxin","citation":{"ista":"Laguri C, Silipo A, Martorana AM, Schanda P, Marchetti R, Polissi A, Molinaro A, Simorre J-P. 2018. Solid state NMR studies of intact lipopolysaccharide endotoxin. ACS Chemical Biology. 13(8), 2106–2113.","ieee":"C. Laguri <i>et al.</i>, “Solid state NMR studies of intact lipopolysaccharide endotoxin,” <i>ACS Chemical Biology</i>, vol. 13, no. 8. American Chemical Society, pp. 2106–2113, 2018.","chicago":"Laguri, Cedric, Alba Silipo, Alessandra M. Martorana, Paul Schanda, Roberta Marchetti, Alessandra Polissi, Antonio Molinaro, and Jean-Pierre Simorre. “Solid State NMR Studies of Intact Lipopolysaccharide Endotoxin.” <i>ACS Chemical Biology</i>. American Chemical Society, 2018. <a href=\"https://doi.org/10.1021/acschembio.8b00271\">https://doi.org/10.1021/acschembio.8b00271</a>.","mla":"Laguri, Cedric, et al. “Solid State NMR Studies of Intact Lipopolysaccharide Endotoxin.” <i>ACS Chemical Biology</i>, vol. 13, no. 8, American Chemical Society, 2018, pp. 2106–13, doi:<a href=\"https://doi.org/10.1021/acschembio.8b00271\">10.1021/acschembio.8b00271</a>.","short":"C. Laguri, A. Silipo, A.M. Martorana, P. Schanda, R. Marchetti, A. Polissi, A. Molinaro, J.-P. Simorre, ACS Chemical Biology 13 (2018) 2106–2113.","apa":"Laguri, C., Silipo, A., Martorana, A. M., Schanda, P., Marchetti, R., Polissi, A., … Simorre, J.-P. (2018). Solid state NMR studies of intact lipopolysaccharide endotoxin. <i>ACS Chemical Biology</i>. American Chemical Society. <a href=\"https://doi.org/10.1021/acschembio.8b00271\">https://doi.org/10.1021/acschembio.8b00271</a>","ama":"Laguri C, Silipo A, Martorana AM, et al. Solid state NMR studies of intact lipopolysaccharide endotoxin. <i>ACS Chemical Biology</i>. 2018;13(8):2106-2113. doi:<a href=\"https://doi.org/10.1021/acschembio.8b00271\">10.1021/acschembio.8b00271</a>"},"year":"2018","oa_version":"None","type":"journal_article","author":[{"full_name":"Laguri, Cedric","first_name":"Cedric","last_name":"Laguri"},{"last_name":"Silipo","first_name":"Alba","full_name":"Silipo, Alba"},{"full_name":"Martorana, Alessandra M.","first_name":"Alessandra M.","last_name":"Martorana"},{"full_name":"Schanda, Paul","first_name":"Paul","last_name":"Schanda","id":"7B541462-FAF6-11E9-A490-E8DFE5697425","orcid":"0000-0002-9350-7606"},{"full_name":"Marchetti, Roberta","first_name":"Roberta","last_name":"Marchetti"},{"first_name":"Alessandra","full_name":"Polissi, Alessandra","last_name":"Polissi"},{"full_name":"Molinaro, Antonio","first_name":"Antonio","last_name":"Molinaro"},{"first_name":"Jean-Pierre","full_name":"Simorre, Jean-Pierre","last_name":"Simorre"}],"day":"02","article_type":"original"},{"article_type":"original","year":"2017","has_accepted_license":"1","oa_version":"Published Version","external_id":{"pmid":["29119945"]},"scopus_import":"1","date_updated":"2021-11-29T09:28:14Z","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","publication_identifier":{"issn":["2050-084X"]},"article_processing_charge":"No","article_number":"e30292","file":[{"success":1,"date_created":"2021-11-29T09:07:41Z","content_type":"application/pdf","file_id":"10372","relation":"main_file","date_updated":"2021-11-29T09:07:41Z","access_level":"open_access","checksum":"c35f42dcfb007f6d6c761a27e24c26d3","file_name":"2017_eLife_Helle.pdf","creator":"cchlebak","file_size":6120157}],"date_published":"2017-11-09T00:00:00Z","_id":"10370","abstract":[{"lang":"eng","text":"Eukaryotic cells are densely packed with macromolecular complexes and intertwining organelles, continually transported and reshaped. Intriguingly, organelles avoid clashing and entangling with each other in such limited space. Mitochondria form extensive networks constantly remodeled by fission and fusion. Here, we show that mitochondrial fission is triggered by mechanical forces. Mechano-stimulation of mitochondria – via encounter with motile intracellular pathogens, via external pressure applied by an atomic force microscope, or via cell migration across uneven microsurfaces – results in the recruitment of the mitochondrial fission machinery, and subsequent division. We propose that MFF, owing to affinity for narrow mitochondria, acts as a membrane-bound force sensor to recruit the fission machinery to mechanically strained sites. Thus, mitochondria adapt to the environment by sensing and responding to biomechanical cues. Our findings that mechanical triggers can be coupled to biochemical responses in membrane dynamics may explain how organelles orderly cohabit in the crowded cytoplasm."}],"publication_status":"published","main_file_link":[{"open_access":"1","url":"https://elifesciences.org/articles/30292"}],"oa":1,"file_date_updated":"2021-11-29T09:07:41Z","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","image":"/images/cc_by.png","short":"CC BY (4.0)"},"volume":6,"citation":{"short":"S.C.J. Helle, Q. Feng, M.J. Aebersold, L. Hirt, R.R. Grüter, A. Vahid, A. Sirianni, S. Mostowy, J.G. Snedeker, A. Šarić, T. Idema, T. Zambelli, B. Kornmann, ELife 6 (2017).","ama":"Helle SCJ, Feng Q, Aebersold MJ, et al. Mechanical force induces mitochondrial fission. <i>eLife</i>. 2017;6. doi:<a href=\"https://doi.org/10.7554/elife.30292\">10.7554/elife.30292</a>","apa":"Helle, S. C. J., Feng, Q., Aebersold, M. J., Hirt, L., Grüter, R. R., Vahid, A., … Kornmann, B. (2017). Mechanical force induces mitochondrial fission. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/elife.30292\">https://doi.org/10.7554/elife.30292</a>","chicago":"Helle, Sebastian Carsten Johannes, Qian Feng, Mathias J Aebersold, Luca Hirt, Raphael R Grüter, Afshin Vahid, Andrea Sirianni, et al. “Mechanical Force Induces Mitochondrial Fission.” <i>ELife</i>. eLife Sciences Publications, 2017. <a href=\"https://doi.org/10.7554/elife.30292\">https://doi.org/10.7554/elife.30292</a>.","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.","ieee":"S. C. J. Helle <i>et al.</i>, “Mechanical force induces mitochondrial fission,” <i>eLife</i>, vol. 6. eLife Sciences Publications, 2017.","mla":"Helle, Sebastian Carsten Johannes, et al. “Mechanical Force Induces Mitochondrial Fission.” <i>ELife</i>, vol. 6, e30292, eLife Sciences Publications, 2017, doi:<a href=\"https://doi.org/10.7554/elife.30292\">10.7554/elife.30292</a>."},"title":"Mechanical force induces mitochondrial fission","day":"09","type":"journal_article","author":[{"full_name":"Helle, Sebastian Carsten Johannes","first_name":"Sebastian Carsten Johannes","last_name":"Helle"},{"last_name":"Feng","full_name":"Feng, Qian","first_name":"Qian"},{"last_name":"Aebersold","full_name":"Aebersold, Mathias J","first_name":"Mathias J"},{"first_name":"Luca","full_name":"Hirt, Luca","last_name":"Hirt"},{"last_name":"Grüter","full_name":"Grüter, Raphael R","first_name":"Raphael R"},{"last_name":"Vahid","full_name":"Vahid, Afshin","first_name":"Afshin"},{"last_name":"Sirianni","first_name":"Andrea","full_name":"Sirianni, Andrea"},{"last_name":"Mostowy","full_name":"Mostowy, Serge","first_name":"Serge"},{"first_name":"Jess G","full_name":"Snedeker, Jess G","last_name":"Snedeker"},{"id":"bf63d406-f056-11eb-b41d-f263a6566d8b","orcid":"0000-0002-7854-2139","full_name":"Šarić, Anđela","first_name":"Anđela","last_name":"Šarić"},{"last_name":"Idema","first_name":"Timon","full_name":"Idema, Timon"},{"last_name":"Zambelli","full_name":"Zambelli, Tomaso","first_name":"Tomaso"},{"first_name":"Benoît","full_name":"Kornmann, Benoît","last_name":"Kornmann"}],"pmid":1,"keyword":["general immunology and microbiology","general biochemistry","genetics and molecular biology","general medicine","general neuroscience"],"language":[{"iso":"eng"}],"ddc":["572"],"doi":"10.7554/elife.30292","month":"11","extern":"1","date_created":"2021-11-29T08:51:38Z","publisher":"eLife Sciences Publications","publication":"eLife","quality_controlled":"1","intvolume":"         6","status":"public"},{"acknowledgement":"This work was supported by the National Sciences and Engineering Research Council of Canada [Canada Graduate\r\nScholarship–Doctoral to K.J.; Discovery Grant to X.L.]; the department of Botany at the University of f British Columbia\r\n[the Dewar Cooper Memorial Fund to X.L.].The authors would like to thank Dr. Yuelin Zhang and Ms. Yan Li for their assistance with next-generation sequencing, and Mr. Charles Copeland for critical reading of the manuscript.","pmid":1,"doi":"10.1093/pcp/pcv087","language":[{"iso":"eng"}],"keyword":["Cell Biology","Plant Science","Physiology","General Medicine"],"title":"The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity","citation":{"apa":"Johnson, K. C. M., Xia, S., Feng, X., &#38; Li, X. (2015). The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity. <i>Plant and Cell Physiology</i>. Oxford University Press. <a href=\"https://doi.org/10.1093/pcp/pcv087\">https://doi.org/10.1093/pcp/pcv087</a>","ama":"Johnson KCM, Xia S, Feng X, Li X. The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity. <i>Plant and Cell Physiology</i>. 2015;56(8):1616-1623. doi:<a href=\"https://doi.org/10.1093/pcp/pcv087\">10.1093/pcp/pcv087</a>","short":"K.C.M. Johnson, S. Xia, X. Feng, X. Li, Plant and Cell Physiology 56 (2015) 1616–1623.","mla":"Johnson, Kaeli C. M., et al. “The Chromatin Remodeler SPLAYED Negatively Regulates SNC1-Mediated Immunity.” <i>Plant and Cell Physiology</i>, vol. 56, no. 8, Oxford University Press, 2015, pp. 1616–23, doi:<a href=\"https://doi.org/10.1093/pcp/pcv087\">10.1093/pcp/pcv087</a>.","ista":"Johnson KCM, Xia S, Feng X, Li X. 2015. The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity. Plant and Cell Physiology. 56(8), 1616–1623.","ieee":"K. C. M. Johnson, S. Xia, X. Feng, and X. Li, “The chromatin remodeler SPLAYED negatively regulates SNC1-mediated immunity,” <i>Plant and Cell Physiology</i>, vol. 56, no. 8. Oxford University Press, pp. 1616–1623, 2015.","chicago":"Johnson, Kaeli C.M., Shitou Xia, Xiaoqi Feng, and Xin Li. “The Chromatin Remodeler SPLAYED Negatively Regulates SNC1-Mediated Immunity.” <i>Plant and Cell Physiology</i>. Oxford University Press, 2015. <a href=\"https://doi.org/10.1093/pcp/pcv087\">https://doi.org/10.1093/pcp/pcv087</a>."},"author":[{"first_name":"Kaeli C.M.","full_name":"Johnson, Kaeli C.M.","last_name":"Johnson"},{"full_name":"Xia, Shitou","first_name":"Shitou","last_name":"Xia"},{"orcid":"0000-0002-4008-1234","id":"e0164712-22ee-11ed-b12a-d80fcdf35958","last_name":"Feng","full_name":"Feng, Xiaoqi","first_name":"Xiaoqi"},{"last_name":"Li","full_name":"Li, Xin","first_name":"Xin"}],"type":"journal_article","publisher":"Oxford University Press","status":"public","intvolume":"        56","quality_controlled":"1","department":[{"_id":"XiFe"}],"publication":"Plant and Cell Physiology","page":"1616-1623","date_created":"2023-01-16T09:20:22Z","extern":"1","month":"08","publication_identifier":{"issn":["0032-0781","1471-9053"]},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","date_updated":"2023-05-08T11:03:23Z","external_id":{"pmid":["26063389"]},"scopus_import":"1","year":"2015","oa_version":"None","article_type":"original","publication_status":"published","volume":56,"issue":"8","article_processing_charge":"No","date_published":"2015-08-01T00:00:00Z","_id":"12196","abstract":[{"lang":"eng","text":"SNC1 (SUPPRESSOR OF NPR1, CONSTITUTIVE 1) is one of a suite of intracellular Arabidopsis NOD-like receptor (NLR) proteins which, upon activation, result in the induction of defense responses. However, the molecular mechanisms underlying NLR activation and the subsequent provocation of immune responses are only partially characterized. To identify negative regulators of NLR-mediated immunity, a forward genetic screen was undertaken to search for enhancers of the dwarf, autoimmune gain-of-function snc1 mutant. To avoid lethality resulting from severe dwarfism, the screen was conducted using mos4 (modifier of snc1, 4) snc1 plants, which display wild-type-like morphology and resistance. M2 progeny were screened for mutant, snc1-enhancing (muse) mutants displaying a reversion to snc1-like phenotypes. The muse9 mos4 snc1 triple mutant was found to exhibit dwarf morphology, elevated expression of the pPR2-GUS defense marker reporter gene and enhanced resistance to the oomycete pathogen Hyaloperonospora arabidopsidis Noco2. Via map-based cloning and Illumina sequencing, it was determined that the muse9 mutation is in the gene encoding the SWI/SNF chromatin remodeler SYD (SPLAYED), and was thus renamed syd-10. The syd-10 single mutant has no observable alteration from wild-type-like resistance, although the syd-4 T-DNA insertion allele displays enhanced resistance to the bacterial pathogen Pseudomonas syringae pv. maculicola ES4326. Transcription of SNC1 is increased in both syd-4 and syd-10. These data suggest that SYD plays a subtle, specific role in the regulation of SNC1 expression and SNC1-mediated immunity. SYD may work with other proteins at the chromatin level to repress SNC1 transcription; such regulation is important for fine-tuning the expression of NLR-encoding genes to prevent unpropitious autoimmunity."}]},{"scopus_import":"1","keyword":["General Medicine"],"date_updated":"2023-09-05T14:19:47Z","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","language":[{"iso":"eng"}],"publication_identifier":{"issn":["0012-0456"],"eissn":["1869-7135"]},"doi":"10.1365/s13291-014-0083-9","citation":{"short":"R. Seiringer, Jahresbericht Der Deutschen Mathematiker-Vereinigung 116 (2014) 21–41.","apa":"Seiringer, R. (2014). The excitation spectrum for Bose fluids with weak interactions. <i>Jahresbericht Der Deutschen Mathematiker-Vereinigung</i>. Springer Nature. <a href=\"https://doi.org/10.1365/s13291-014-0083-9\">https://doi.org/10.1365/s13291-014-0083-9</a>","ama":"Seiringer R. The excitation spectrum for Bose fluids with weak interactions. <i>Jahresbericht der Deutschen Mathematiker-Vereinigung</i>. 2014;116:21-41. doi:<a href=\"https://doi.org/10.1365/s13291-014-0083-9\">10.1365/s13291-014-0083-9</a>","ista":"Seiringer R. 2014. The excitation spectrum for Bose fluids with weak interactions. Jahresbericht der Deutschen Mathematiker-Vereinigung. 116, 21–41.","ieee":"R. Seiringer, “The excitation spectrum for Bose fluids with weak interactions,” <i>Jahresbericht der Deutschen Mathematiker-Vereinigung</i>, vol. 116. Springer Nature, pp. 21–41, 2014.","chicago":"Seiringer, Robert. “The Excitation Spectrum for Bose Fluids with Weak Interactions.” <i>Jahresbericht Der Deutschen Mathematiker-Vereinigung</i>. Springer Nature, 2014. <a href=\"https://doi.org/10.1365/s13291-014-0083-9\">https://doi.org/10.1365/s13291-014-0083-9</a>.","mla":"Seiringer, Robert. “The Excitation Spectrum for Bose Fluids with Weak Interactions.” <i>Jahresbericht Der Deutschen Mathematiker-Vereinigung</i>, vol. 116, Springer Nature, 2014, pp. 21–41, doi:<a href=\"https://doi.org/10.1365/s13291-014-0083-9\">10.1365/s13291-014-0083-9</a>."},"title":"The excitation spectrum for Bose fluids with weak interactions","article_type":"original","day":"01","type":"journal_article","author":[{"last_name":"Seiringer","full_name":"Seiringer, Robert","first_name":"Robert","id":"4AFD0470-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-6781-0521"}],"oa_version":"None","year":"2014","publication_status":"published","publisher":"Springer Nature","publication":"Jahresbericht der Deutschen Mathematiker-Vereinigung","quality_controlled":"1","department":[{"_id":"RoSe"}],"status":"public","intvolume":"       116","volume":116,"page":"21-41","article_processing_charge":"No","month":"03","date_published":"2014-03-01T00:00:00Z","_id":"10814","abstract":[{"text":"We review recent progress towards a rigorous understanding of the excitation spectrum of bosonic quantum many-body systems. In particular, we explain how one can rigorously establish the predictions resulting from the Bogoliubov approximation in the mean field limit. The latter predicts that the spectrum is made up of elementary excitations, whose energy behaves linearly in the momentum for small momentum. This property is crucial for the superfluid behavior of the system. We also discuss a list of open problems in this field.","lang":"eng"}],"date_created":"2022-03-04T07:54:39Z"},{"oa":1,"main_file_link":[{"open_access":"1","url":"https://doi.org/10.1111/cga.12039"}],"publication_status":"published","volume":54,"issue":"1","article_processing_charge":"No","_id":"10815","date_published":"2014-02-01T00:00:00Z","abstract":[{"text":"In the last several decades, developmental biology has clarified the molecular mechanisms of embryogenesis and organogenesis. In particular, it has demonstrated that the “tool-kit genes” essential for regulating developmental processes are not only highly conserved among species, but are also used as systems at various times and places in an organism to control distinct developmental events. Therefore, mutations in many of these tool-kit genes may cause congenital diseases involving morphological abnormalities. This link between genes and abnormal morphological phenotypes underscores the importance of understanding how cells behave and contribute to morphogenesis as a result of gene function. Recent improvements in live imaging and in quantitative analyses of cellular dynamics will advance our understanding of the cellular pathogenesis of congenital diseases associated with aberrant morphologies. In these studies, it is critical to select an appropriate model organism for the particular phenomenon of interest.","lang":"eng"}],"publication_identifier":{"issn":["0914-3505"]},"date_updated":"2022-03-04T08:26:05Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","scopus_import":"1","external_id":{"pmid":["24666178"]},"year":"2014","oa_version":"None","article_type":"original","publisher":"Wiley","status":"public","intvolume":"        54","quality_controlled":"1","department":[{"_id":"CaHe"}],"publication":"Congenital Anomalies","page":"1-7","date_created":"2022-03-04T08:17:25Z","month":"02","acknowledgement":"The authors thank all the members of the Division of Morphogenesis, National Institute for Basic Biology, for their contributions to the research, their encouragement, and helpful discussions, particularly Dr M. Suzuki for his critical reading of the manuscript. We also thank the Model Animal Research and Spectrography and Bioimaging Facilities, NIBB Core Research Facilities, for technical support. M.H. was supported by a research fellowship from the Japan Society for the Promotion of Science (JSPS). Our work introduced in this review was supported by a Grant-in-Aid for Scientific Research on Innovative Areas from the Ministry of Education, Culture, Sports, Science, and Technology (MEXT), Japan, to N.U.","pmid":1,"doi":"10.1111/cga.12039","language":[{"iso":"eng"}],"keyword":["Developmental Biology","Embryology","General Medicine","Pediatrics","Perinatology","and Child Health"],"title":"Molecular and cellular mechanisms of development underlying congenital diseases","citation":{"short":"M. Hashimoto, H. Morita, N. Ueno, Congenital Anomalies 54 (2014) 1–7.","ama":"Hashimoto M, Morita H, Ueno N. Molecular and cellular mechanisms of development underlying congenital diseases. <i>Congenital Anomalies</i>. 2014;54(1):1-7. doi:<a href=\"https://doi.org/10.1111/cga.12039\">10.1111/cga.12039</a>","apa":"Hashimoto, M., Morita, H., &#38; Ueno, N. (2014). Molecular and cellular mechanisms of development underlying congenital diseases. <i>Congenital Anomalies</i>. Wiley. <a href=\"https://doi.org/10.1111/cga.12039\">https://doi.org/10.1111/cga.12039</a>","chicago":"Hashimoto, Masakazu, Hitoshi Morita, and Naoto Ueno. “Molecular and Cellular Mechanisms of Development Underlying Congenital Diseases.” <i>Congenital Anomalies</i>. Wiley, 2014. <a href=\"https://doi.org/10.1111/cga.12039\">https://doi.org/10.1111/cga.12039</a>.","ista":"Hashimoto M, Morita H, Ueno N. 2014. Molecular and cellular mechanisms of development underlying congenital diseases. Congenital Anomalies. 54(1), 1–7.","ieee":"M. Hashimoto, H. Morita, and N. Ueno, “Molecular and cellular mechanisms of development underlying congenital diseases,” <i>Congenital Anomalies</i>, vol. 54, no. 1. Wiley, pp. 1–7, 2014.","mla":"Hashimoto, Masakazu, et al. “Molecular and Cellular Mechanisms of Development Underlying Congenital Diseases.” <i>Congenital Anomalies</i>, vol. 54, no. 1, Wiley, 2014, pp. 1–7, doi:<a href=\"https://doi.org/10.1111/cga.12039\">10.1111/cga.12039</a>."},"type":"journal_article","author":[{"last_name":"Hashimoto","full_name":"Hashimoto, Masakazu","first_name":"Masakazu"},{"last_name":"Morita","first_name":"Hitoshi","full_name":"Morita, Hitoshi","id":"4C6E54C6-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Naoto","full_name":"Ueno, Naoto","last_name":"Ueno"}],"day":"01"}]