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dc.contributor.author | Pacheco, Sarai | |
dc.contributor.author | Maldonado-Linares, Andros | |
dc.contributor.author | Marcet-Ortega, Marina | |
dc.contributor.author | Rojas, Cristina | |
dc.contributor.author | Martínez-Marchal, Ana | |
dc.contributor.author | Fuentes-Lazaro, Judit | |
dc.contributor.author | Lange, Julian | |
dc.contributor.author | Jasin, Maria | |
dc.contributor.author | Keeney, Scott | |
dc.contributor.author | Fernandez-Capetillo, Oscar | |
dc.contributor.author | Garcia-Caldés, Montserrat | |
dc.contributor.author | Roig, Ignasi | |
dc.date.accessioned | 2019-09-16T10:27:58Z | |
dc.date.available | 2019-09-16T10:27:58Z | |
dc.date.issued | 2018-07-05 | |
dc.identifier.citation | Nat Commun. 2018;9(1):2622. | es_ES |
dc.identifier.issn | 2041-1723 | es_ES |
dc.identifier.uri | http://hdl.handle.net/20.500.12105/8349 | |
dc.description.abstract | Precise execution of recombination during meiosis is essential for forming chromosomally-balanced gametes. Meiotic recombination initiates with the formation and resection of DNA double-strand breaks (DSBs). Cellular responses to meiotic DSBs are critical for efficient repair and quality control, but molecular features of these remain poorly understood, particularly in mammals. Here we report that the DNA damage response protein kinase ATR is crucial for meiotic recombination and completion of meiotic prophase in mice. Using a hypomorphic Atr mutation and pharmacological inhibition of ATR in vivo and in cultured spermatocytes, we show that ATR, through its effector kinase CHK1, promotes efficient RAD51 and DMC1 assembly at RPA-coated resected DSB sites and establishment of interhomolog connections during meiosis. Furthermore, our findings suggest that ATR promotes local accumulation of recombination markers on unsynapsed axes during meiotic prophase to favor homologous chromosome synapsis. These data reveal that ATR plays multiple roles in mammalian meiotic recombination. | es_ES |
dc.description.sponsorship | We thank M. A. Handel (The Jackson Laboratory, Bar Harbor, USA) for the anti-H1T antibody; E. Marcon for the anti-RPA antibody (University of Toronto, Canada); A. Toth for the anti-pHORMAD2 antibody (U. Dresden, Germany) and N. Hunter for the anti- RNF212 antibody (UC Davis, USA); J. Turner (National Institute for Medical Research,London, UK) for assistance in the RNA-FISH experiments, for the X chromosome probe,for providing AtrFL/−testis samples and for sharing unpublished data; L. Kauppi(University of Helsinki, Finland) for providing us with protocols for the testis cultures;and members of the Roig lab and the Spanish Ministerio de Ciencia e Innovación-funded Network of Spanish groups working on Meiosis (MeioNet, BFU201‐71786‐REDT) and Enrique Martínez Pérez (Imperial College, London, UK) for helpful discussions. M.M.O. was supported by a FPI fellowship from the Ministerio de Ciencia e Innovación (BES-2011-045381). J.L. was supported in part by American Cancer Society post-doctoral fellowship (PF-12-157-01-DMC). S.K. is an Investigator of the Howard Hughes Medical Institute. This work was supported by the Ministerio de Ciencia e Innovación (BFU2010-18965, BFU2013-43965-P and BFU2016-80370-P, I.R.), by the UAB-Aposta award to young investigators (APOSTA2011-03, I.R.) and by the NIH (R35 GM118175, to M.J.and R35 GM118092 to S.K.). | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Nature Publishing Group | es_ES |
dc.type.hasVersion | VoR | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-sa/4.0/ | * |
dc.subject.mesh | Animals | es_ES |
dc.subject.mesh | Ataxia Telangiectasia Mutated Proteins | es_ES |
dc.subject.mesh | Cell Cycle Proteins | es_ES |
dc.subject.mesh | Checkpoint Kinase 1 | es_ES |
dc.subject.mesh | Chromosome Pairing | es_ES |
dc.subject.mesh | In Situ Hybridization, Fluorescence | es_ES |
dc.subject.mesh | Male | es_ES |
dc.subject.mesh | Meiosis | es_ES |
dc.subject.mesh | Mice, 129 Strain | es_ES |
dc.subject.mesh | Mice, Inbred C57BL | es_ES |
dc.subject.mesh | Mice, Knockout | es_ES |
dc.subject.mesh | Nuclear Proteins | es_ES |
dc.subject.mesh | Rad51 Recombinase | es_ES |
dc.subject.mesh | Spermatocytes | es_ES |
dc.subject.mesh | Testis | es_ES |
dc.subject.mesh | DNA Breaks, Double-Stranded | es_ES |
dc.subject.mesh | Homologous Recombination | es_ES |
dc.title | ATR is required to complete meiotic recombination in mice | es_ES |
dc.type | journal article | es_ES |
dc.rights.license | Atribución-NoComercial-CompartirIgual 4.0 Internacional | * |
dc.identifier.pubmedID | 29977027 | es_ES |
dc.format.volume | 9 | es_ES |
dc.format.number | 1 | es_ES |
dc.format.page | 2622 | es_ES |
dc.identifier.doi | 10.1038/s41467-018-04851-z | es_ES |
dc.contributor.funder | Ministerio de Ciencia e Innovación (España) | |
dc.contributor.funder | American Cancer Society | |
dc.contributor.funder | Howard Hughes Medical Institute | |
dc.contributor.funder | National Institutes of Health (Estados Unidos) | |
dc.description.peerreviewed | Sí | es_ES |
dc.identifier.e-issn | 2041-1723 | es_ES |
dc.relation.publisherversion | https://doi.org/10.1038/s41467-018-04851-z. | es_ES |
dc.identifier.journal | Nature communications | es_ES |
dc.repisalud.institucion | CNIO | es_ES |
dc.repisalud.orgCNIO | CNIO::Grupos de investigación::Grupo de Inestabilidad Genómica | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/BFU2015-71786-REDT | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/BES-2011-045381 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/BFU2010-18965 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/BFU2013-43965-P | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/ES/BFU2016-80370-P | es_ES |
dc.rights.accessRights | open access | es_ES |