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dc.contributor.authorGodwin, James
dc.contributor.authorGovindasamy, Mohan
dc.contributor.authorMedounsejian, Kiruba
dc.contributor.authorMarch, Eduardo
dc.contributor.authorHalton, Ronan
dc.contributor.authorBourbousse, Ciara
dc.contributor.authorWolf, Léa
dc.contributor.authorFort, Antoine
dc.contributor.authorKrzyszton, Michal
dc.contributor.authorLópez Corrales, Jesús
dc.contributor.authorSwiezewski, Szymon
dc.contributor.authorBarneche, Fredy
dc.contributor.authorSchubert, Daniel
dc.contributor.authorFarrona, Sara
dc.date.accessioned2024-02-13T11:44:31Z
dc.date.available2024-02-13T11:44:31Z
dc.date.copyright2024
dc.date.issued2024-01-22
dc.identifier.citationGodwin, J., Govindasamy, M., Nedounsejian, K., March, E., Halton, R., Bourbousse, C., Wolf, L., Fort, A., M. Krzyszton, M., Corrales, J.L., Swiezewski, S., Barneche, F., Schubert, D., Farrona, S. (2024). The UBP5 histone H2A deubiquitinase counteracts PRCs-mediated repression to regulate Arabidopsis development. 22 January. https://doi.org/10.1038/s41467-023-44546-8en_US
dc.identifier.issn2041-1723
dc.identifier.urihttps://research.thea.ie/handle/20.500.12065/4730
dc.description.abstractPolycomb Repressive Complexes (PRCs) control gene expression through the incorporation of H2Aub and H3K27me3. In recent years, there is increasing evidence of the complexity of PRCs’ interaction networks and the interplay of these interactors with PRCs in epigenome reshaping, which is fundamental to understand gene regulatory mechanisms. Here, we identified UBIQUITIN SPECIFIC PROTEASE 5 (UBP5) as a chromatin player able to counteract the deposition of the two PRCs’ epigenetic hallmarks in Arabidopsis thaliana. We demonstrated that UBP5 is a plant developmental regulator based on functional analyses of ubp5-CRISPR Cas9 mutant plants. UBP5 promotes H2A monoubiquitination erasure, leading to transcriptional de-repression. Furthermore, preferential association of UBP5 at PRC2 recruiting motifs and local H3K27me3 gaining in ubp5 mutant plants suggest the existence of functional interplays between UBP5 and PRC2 in regulating epigenome dynamics. In summary, acting as an antagonist of the pivotal epigenetic repressive marks H2Aub and H3K27me3, UBP5 provides novel insights to disentangle the complex regulation of PRCs’ activities.en_US
dc.formatPDFen_US
dc.language.isoengen_US
dc.publisherNature Researchen_US
dc.relation.ispartofNature Communicationsen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subjectPolycomb Repressive Complexes (PRCs)en_US
dc.subjectGene expressionen_US
dc.subjectGene regulatory mechanismsen_US
dc.subjectUBP5en_US
dc.titleThe UBP5 histone H2A deubiquitinase counteracts PRCs-mediated repression to regulate Arabidopsis developmenten_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.contributor.affiliationTechnological University of the Shannon: Midlands Midwesten_US
dc.contributor.sponsorS.F. acknowledges support from the College of Science and Engineering and the Research Office (University of Galway). S.F. is grateful to Jennifer Siobal for technical support. S.F. thanksMiguel de Lucas Torres (Durham University) for his supportwith Y2H experiments. S.F., R.H., K.N. and M.G. were supported by 20/FFP-P/8693 grant from Science Foundation Ireland (SFI) and by a NUI Galway Research Grant for Returning Academic Careers QA151.M.G. was also supported by the SFI Centre for Research Training in Genomics Data Science (grantN. 18/CRT/6214). J.G. was supported through the University of Galway Hardiman Scholarship programme and Thomas Crawford Research Grant. J.G. internship at IBENS was supported by the COST Action CA16212 INDEPTH (EU). E.M. was funded by a College of Science and Engineering scholarship (University of Galway).Work in FB and CB laboratory was supported by ANR- 18-CE13-0004-01 and ANR-20-CE13-0028 grants from the French National Research Agency. S.S. was supported by Foundation for Polish Science (TEAM POIR.04.04.00-00-3C97/16) and by Polish National Science Centre (SONATA BIS UMO-2018/30/E/NZ1/00354). M.K. was supported by Polish National Science Centre (OPUS UMO-2021/41/B/ NZ3/02605).en_US
dc.description.peerreviewyesen_US
dc.identifier.doi10.1038/s41467-023-44546-8en_US
dc.identifier.orcidhttps://orcid.org/0000-0002-2210-7234en_US
dc.rights.accessrightsinfo:eu-repo/semantics/openAccessen_US
dc.subject.departmentDepartment of Veterinary and Microbial Sciences: TUS Midlandsen_US
dc.type.versioninfo:eu-repo/semantics/publishedVersionen_US


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Attribution 3.0 United States
Except where otherwise noted, this item's license is described as Attribution 3.0 United States