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dc.creatorCano Linares, María Isabeles
dc.creatorYáñez Vilches, Auroraes
dc.creatorGarcía Rodríguez, Néstores
dc.creatorBarrientos Moreno, Martaes
dc.creatorGonzález Prieto, Románes
dc.creatorSan Segundo, Pedroes
dc.creatorUlrich, Helle D.es
dc.creatorPrado, Félixes
dc.date.accessioned2021-09-23T13:26:23Z
dc.date.available2021-09-23T13:26:23Z
dc.date.issued2021
dc.identifier.citationCano Linares, M.I., Yáñez Vilches, A., García Rodríguez, N., Barrientos Moreno, M., González Prieto, R., San Segundo, P.,...,Prado, F. (2021). Non-recombinogenic roles for Rad52 in translesion synthesis during DNA damage tolerance. EMBO Reports, 22 (1), e50410.
dc.identifier.issn1469-221Xes
dc.identifier.issn1469-3178es
dc.identifier.urihttps://hdl.handle.net/11441/126130
dc.description.abstractDNA damage tolerance relies on homologous recombination (HR) and translesion synthesis (TLS) mechanisms to fill in the ssDNA gaps generated during passing of the replication fork over DNA lesions in the template. Whereas TLS requires specialized polymerases able to incorporate a dNTP opposite the lesion and is error-prone, HR uses the sister chromatid and is mostly error-free. We report that the HR protein Rad52—but not Rad51 and Rad57—acts in concert with the TLS machinery (Rad6/Rad18-mediated PCNA ubiquitylation and polymerases Rev1/Pol ζ) to repair MMS and UV light-induced ssDNA gaps through a non-recombinogenic mechanism, as inferred from the different phenotypes displayed in the absence of Rad52 and Rad54 (essential for MMS- and UV-induced HR); accordingly, Rad52 is required for efficient DNA damage-induced mutagenesis. In addition, Rad52, Rad51, and Rad57, but not Rad54, facilitate Rad6/Rad18 binding to chromatin and subsequent DNA damage-induced PCNA ubiquitylation. Therefore, Rad52 facilitates the tolerance process not only by HR but also by TLS through Rad51/Rad57-dependent and -independent processes, providing a novel role for the recombination proteins in maintaining genome integrity.es
dc.description.sponsorshipGobierno de España BFU2015-63698-P, PGC2018-099182-B-I00, BFU2015-65417-R, RTI2018-099055-B-I00, BFU2015-69142-REDTes
dc.description.sponsorshipEuropean Research Council ERC-AdG323179es
dc.formatapplication/pdfes
dc.format.extent20 p.es
dc.language.isoenges
dc.publisherWiley-Blackwelles
dc.relation.ispartofEMBO Reports, 22 (1), e50410.
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectDNA damage tolerancees
dc.subjectHomologous recombinationes
dc.subjectRad52es
dc.subjectTemplate switchinges
dc.subjectTranslesion synthesises
dc.titleNon-recombinogenic roles for Rad52 in translesion synthesis during DNA damage tolerancees
dc.typeinfo:eu-repo/semantics/articlees
dc.type.versioninfo:eu-repo/semantics/publishedVersiones
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.contributor.affiliationUniversidad de Sevilla. Departamento de Genéticaes
dc.relation.projectIDBFU2015-63698-Pes
dc.relation.projectIDPGC2018-099182-B-I00es
dc.relation.projectIDBFU2015-65417-Res
dc.relation.projectIDRTI2018-099055-B-I00es
dc.relation.projectIDBFU2015-69142-REDTes
dc.relation.projectIDERC-AdG323179es
dc.relation.publisherversionhttps://doi.org/10.15252/embr.202050410es
dc.identifier.doi10.15252/embr.202050410es
dc.journaltitleEMBO Reportses
dc.publication.volumen22es
dc.publication.issue1es
dc.publication.initialPagee50410es

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