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RIF1 is essential for 53BP1-dependent nonhomologous end joining and suppression of DNA double-strand break resection

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dc.contributor.authorChapman, J Ross
dc.contributor.authorBarral, Patricia
dc.contributor.authorVannier, Jean-Baptiste
dc.contributor.authorBorel, Valerie
dc.contributor.authorSteger, Martin
dc.contributor.authorTomas-Loba, Antonia
dc.contributor.authorSartori, Alessandro A
dc.contributor.authorAdams, Ian R
dc.contributor.authorBatista, Facundo D
dc.contributor.authorBoulton, Simon J
dc.contributor.departmentFisiología
dc.date.accessioned2024-02-07T07:48:55Z
dc.date.available2024-02-07T07:48:55Z
dc.date.issued2013-03-07
dc.description©<2013>. This manuscript version is made available under the CC-BY-NC-ND license http://creativecommons.org/licenses/by-nc-nd/4.0/ This document is the Published, version of a Published Work that appeared in final form in [Molecular Cell]. To access the final edited and published work see [https://doi.org/10.1016/j.molcel.2013.01.002]
dc.description.abstractThe appropriate execution of DNA double-strand break (DSB) repair is critical for genome stability and tumor avoidance. 53BP1 and BRCA1 directly influence DSB repair pathway choice by regulating 50 end resection, but how this is achieved remains uncertain. Here we report that Rif1 / mice are severely compromised for 53BP1-dependent class switch recombination (CSR) and fusion of dysfunc- tional telomeres. The inappropriate accumulation of RIF1 at DSBs in S phase is antagonized by BRCA1, and deletion of Rif1 suppresses toxic nonhomolo- gous end joining (NHEJ) induced by PARP inhibition in Brca1-deficient cells. Mechanistically, RIF1 is re- cruited to DSBs via the N-terminal phospho-SQ/TQ domain of 53BP1, and DSBs generated by ionizing radiation or during CSR are hyperresected in the absence of RIF1. Thus, RIF1 and 53BP1 cooperate to block DSB resection to promote NHEJ in G1, which is antagonized by BRCA1 in S phase to ensure a switch of DSB repair mode to homologous recombination.
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dc.format.extent16es
dc.identifier.citationMolecular Cell 49(5):858-871, 2013
dc.identifier.doihttps://doi.org/10.1016/j.molcel.2013.01.002
dc.identifier.issnPrint: 1097-2765
dc.identifier.issnElectronico: 1097-4164
dc.identifier.urihttp://hdl.handle.net/10201/138799
dc.languageenges
dc.publisherCell Presses
dc.relationSwiss National Science Foundation (31003A_135507), Promedica Stiftung, and the Vontobel Foundation. Medical Research Council. Cancer Research UK and are Royal Society Wolfson Research Merit Award Holders. ERC Advanced Investigator Grant (RecMitMei). Long-term fellowship from EMBO. Intra-European fellowship of the Seventh Framework Program from the European Commission (PIEF-GA-2008-220863), Sir Henry Wellcome Fellowship.es
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.subjectRIF1
dc.subject.otherCDU::5 - Ciencias puras y naturales::57 - Ciencias biológicas en general:577 - 577 Bioquímica. Biología molecular. Biofísica
dc.titleRIF1 is essential for 53BP1-dependent nonhomologous end joining and suppression of DNA double-strand break resectiones
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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