dc.creator | García Muse, Tatiana | es |
dc.creator | Galindo Díaz, U. | es |
dc.creator | García Rubio, María Luisa | es |
dc.creator | Martin, Julie S. | es |
dc.creator | Polanowska, Jolanta | es |
dc.creator | O'Reilly, N. | es |
dc.creator | Aguilera López, Andrés | es |
dc.creator | Boulton, Simon J. | es |
dc.date.accessioned | 2019-01-24T15:33:02Z | |
dc.date.available | 2019-01-24T15:33:02Z | |
dc.date.issued | 2019 | |
dc.identifier.citation | García Muse, T., Galindo Díaz, U., García Rubio, M.L., Martin, J.S., Polanowska, J., O'Reilly, N.,...,Boulton, S.J. (2019). A Meiotic Checkpoint Alters Repair Partner Bias to Permit Inter-sister Repair of Persistent DSBs. Cell Reports, 26 (3), 775-787.e5. | |
dc.identifier.issn | 2211-1247 | es |
dc.identifier.uri | https://hdl.handle.net/11441/82040 | |
dc.description.abstract | Accurate meiotic chromosome segregation critically depends on the formation of inter-homolog crossovers initiated by double-strand breaks (DSBs). Inaccuracies in this process can drive aneuploidy and developmental defects, but how meiotic cells are protected from unscheduled DNA breaks remains unexplored. Here we define a checkpoint response to persistent meiotic DSBs in C. elegans that phosphorylates the synaptonemal complex (SC) to switch repair partner from the homolog to the sister chromatid. A key target of this response is the core SC component SYP-1, which is phosphorylated in response to ionizing radiation (IR) or unrepaired meiotic DSBs. Failure to phosphorylate (syp-16A) or dephosphorylate (syp-16D) SYP-1 in response to DNA damage results in chromosome non-dysjunction, hyper-sensitivity to IR-induced DSBs, and synthetic lethality with loss of brc-1BRCA1. Since BRC-1 is required for inter-sister repair, these observations reveal that checkpoint-dependent SYP-1 phosphorylation safeguards the germline against persistent meiotic DSBs by channelling repair to the sister chromatid. | es |
dc.description.sponsorship | Cancer Research UK FC0010048 | es |
dc.description.sponsorship | UK Medical Research Council FC0010048 | es |
dc.description.sponsorship | Wellcome Trust FC0010048 | es |
dc.description.sponsorship | Ministerio de Economía y Competitividad BFU2016-75058-P | es |
dc.description.sponsorship | European Research Council ERC2014 AdG669898 TARLOOP | es |
dc.format | application/pdf | es |
dc.language.iso | eng | es |
dc.publisher | Elsevier B.V. | es |
dc.relation.ispartof | Cell Reports, 26 (3), 775-787.e5. | |
dc.rights | Attribution-NonCommercial-NoDerivatives 4.0 Internacional | * |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | * |
dc.subject | ATR/ATM | es |
dc.subject | BRC-1 | es |
dc.subject | DNA damage response | es |
dc.subject | DNA double-strand breaks | es |
dc.subject | Inter-sister repair | es |
dc.subject | Meiosis | es |
dc.subject | Synaptonemal complex | es |
dc.title | A Meiotic Checkpoint Alters Repair Partner Bias to Permit Inter-sister Repair of Persistent DSBs | es |
dc.type | info:eu-repo/semantics/article | es |
dcterms.identifier | https://ror.org/03yxnpp24 | |
dc.type.version | info:eu-repo/semantics/publishedVersion | es |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | es |
dc.contributor.affiliation | Universidad de Sevilla. Departamento de Genética | es |
dc.relation.projectID | FC0010048 | es |
dc.relation.projectID | FC0010048 | es |
dc.relation.projectID | FC0010048 | es |
dc.relation.projectID | BFU2016-75058-P | es |
dc.relation.projectID | ERC2014 AdG669898 TARLOOP | es |
dc.relation.publisherversion | http://dx.doi.org/10.1016/j.celrep.2018.12.074 | es |
dc.identifier.doi | 10.1016/j.celrep.2018.12.074 | es |
idus.format.extent | 18 p. | es |
dc.journaltitle | Cell Reports | es |
dc.publication.volumen | 26 | es |
dc.publication.issue | 3 | es |
dc.publication.initialPage | 775 | es |
dc.publication.endPage | 787.e5 | es |