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The anaphase promoting complex impacts repair choice by protecting ubiquitin signalling at DNA damage sites

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dc.contributor.authorHa, Kyungsoo
dc.contributor.authorMa, Chengxian
dc.contributor.authorLin, Han
dc.contributor.authorTang, Lichun
dc.contributor.authorLian, Zhusheng
dc.contributor.authorZhao, Fang
dc.contributor.authorLi, Ju-Mei
dc.contributor.authorZhen, Bei
dc.contributor.authorPei, Huadong
dc.contributor.authorHan, Suxia
dc.contributor.authorMalumbres Martinez, Marcos
dc.contributor.authorJin, Jianping
dc.contributor.authorChen, Huan
dc.contributor.authorZhao, Yongxiang
dc.contributor.authorZhu, Qing
dc.contributor.authorZhang, Pumin
dc.contributor.funderNational Institutes of Health (Estados Unidos)
dc.contributor.funderMinistry of Science and Technology (China)
dc.contributor.funderNational Natural Science Foundation of China
dc.contributor.funderWelch Foundation
dc.date.accessioned2018-12-13T11:02:37Z
dc.date.available2018-12-13T11:02:37Z
dc.date.issued2017
dc.description.abstractDouble-strand breaks (DSBs) are repaired through two major pathways, homology-directed recombination (HDR) and non-homologous end joining (NHEJ). While HDR can only occur in S/G2, NHEJ can happen in all cell cycle phases (except mitosis). How then is the repair choice made in S/G2 cells? Here we provide evidence demonstrating that APCCdh1 plays a critical role in choosing the repair pathways in S/G2 cells. Our results suggest that the default for all DSBs is to recruit 53BP1 and RIF1. BRCA1 is blocked from being recruited to broken ends because its recruitment signal, K63-linked poly-ubiquitin chains on histones, is actively destroyed by the deubiquitinating enzyme USP1. We show that the removal of USP1 depends on APCCdh1 and requires Chk1 activation known to be catalysed by ssDNA-RPA-ATR signalling at the ends designated for HDR, linking the status of end processing to RIF1 or BRCA1 recruitment.es_ES
dc.description.peerreviewedSíes_ES
dc.description.sponsorshipWe thank S.-Y. Lin (MD Anderson Cancer Center) for cell lines; J. Rosen (Baylor College of Medicine) for reagents; H. Masai (Tokyo Metropolitan Institute of Medical Science) for U2OS-Fucci cell line; D. Durocher (University of Toronto) for HeLa-Fucci cell line; E. Citterio (Netherlands Cancer Institute) for GFP-USP3 construct; M.S.Y. Huen (The University of Hong Kong) for RNF168 antibody. This work was performed with facilities and instruments in the Imaging Core of National Center for Protein Science (Beijing), the Cytometry and Cell Sorting Core at Baylor College of Medicine with funding from the NIH (P30 AI036211, P30 CA125123 and S10 RR024574), the Integrated Microscopy Core at Baylor College of Medicine with funding from the NIH (HD007495, DK56338 and CA125123), and the John S. Dunn Gulf Coast Consortium for Chemical Genomics. We also thank other members of the Zhang lab for helpful discussion and support. This work was supported in part by an international collaboration grant (# 2013DFB30210) and a 973 Project grant (# 2013CB910300) from Chinese Minister of Science and Technology, in part by a Chinese National Natural Science Foundation grant (# 81171920), in part by a grant from The Committee of Science and Technology of Beijing Municipality, China (# Z141100000214015), and in part by NIH grants CA116097 and CA122623 to P.Z. J.J. is supported by grants from National Institutes of Health (R01GM102529) and the Welch Foundation (AU-1711). S.H. is supported by grants (# 81272488 and 81472795) from Chinese National Natural Science Foundation. Y.Z. is supported by grants from the National Natural Scientific Foundation of China (No. 81430055), Programs for Changjiang Scholars and Innovative Research Team in University (No. IRT_15R13).es_ES
dc.format.page15751es_ES
dc.format.volume8es_ES
dc.identifier.citationNat Commun. 2017; 8:15751.es_ES
dc.identifier.doi10.1038/ncomms15751es_ES
dc.identifier.e-issn2041-1723es_ES
dc.identifier.issn2041-1723es_ES
dc.identifier.journalNature communicationses_ES
dc.identifier.pubmedID28604711es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/6840
dc.language.isoenges_ES
dc.publisherNature Publishing Group
dc.relation.publisherversionhttps://doi.org/10.1038/ncomms15751.es_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Grupos de investigación::Grupo de División Celular y Cánceres_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subject.meshAnaphase-Promoting Complex-Cyclosomees_ES
dc.subject.meshAnimalses_ES
dc.subject.meshCell Linees_ES
dc.subject.meshDNA Breaks, Double-Strandedes_ES
dc.subject.meshDNA Repaires_ES
dc.subject.meshGenomic Instabilityes_ES
dc.subject.meshHEK293 Cellses_ES
dc.subject.meshHeLa Cellses_ES
dc.subject.meshHumanses_ES
dc.subject.meshMicees_ES
dc.subject.meshModels, Genetices_ES
dc.subject.meshSignal Transductiones_ES
dc.subject.meshUbiquitines_ES
dc.subject.meshDNA Damagees_ES
dc.titleThe anaphase promoting complex impacts repair choice by protecting ubiquitin signalling at DNA damage siteses_ES
dc.typejournal articlees_ES
dc.type.hasVersionVoRes_ES
dspace.entity.typePublication
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