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dc.contributor.authorAmaral, Nuno
dc.contributor.authorVendrell, Alexandre
dc.contributor.authorMaier, Michael
dc.contributor.authorKumar, Arun
dc.contributor.authorMendoza, Manuel
dc.contributor.authorFunaya, Charlotta
dc.contributor.authorGeli, María Isabel
dc.contributor.authorIdrissi, Fatima-Zahra
dc.contributor.authorColomina i Gabarrella, Neus
dc.contributor.authorTorres Rosell, Jordi
dc.date.accessioned2017-01-23T12:57:46Z
dc.date.issued2016
dc.identifier.issn0028-0836
dc.identifier.urihttp://hdl.handle.net/10459.1/59075
dc.description.abstractAnaphase chromatin bridges can lead to chromosome breakage if not properly resolved before completion of cytokinesis. The NoCut checkpoint, which depends on Aurora B at the spindle midzone, delays abscission in response to chromosome segregation defects in yeast and animal cells. How chromatin bridges are detected, and whether abscission inhibition prevents their damage, remain key unresolved questions. We find that bridges induced by DNA replication stress and by condensation or decatenation defects, but not dicentric chromosomes, delay abscission in a NoCut-dependent manner. Decatenation and condensation defects lead to spindle stabilization during cytokinesis, allowing bridge detection by Aurora B. NoCut does not prevent DNA damage following condensin or topoisomerase II inactivation; however, it protects anaphase bridges and promotes cellular viability after replication stress. Therefore, the molecular origin of chromatin bridges is critical for activation of NoCut, which plays a key role in the maintenance of genome stability after replicative stress.ca_ES
dc.description.sponsorshipWe thank S. Oliferenko and N. Brownlow for suggestions and critical reading of the manuscript; Y. Barral and D. Pellman for helpful discussions; G. Filion for help with statistical analysis; T. Sanmartin for technical support; the CRG Advanced Light Microscopy Unit; and Y. Schwab (EMBL, Heidelberg), C. López-Iglesias and Y. Muela-Castro (CCIT University of Barcelona) for assistance with electron microscopy. This research was supported by `La Caixa' fellowships to N.A., G.N. and M.Maier, and grants from the Spanish Ministry of Economy and Competitivity (BFU2011-30185 and CDS2009-00016 to M.-I.G.; BFU2015-71308 and BFU2013-50245-EXP to J.T.-R.; and BFU2009-08213 and BFU2012-37162 to M.Mendoza), and from the European Research Council (ERC Starting Grant 260965 to M.Mendoza). We acknowledge support from the Spanish Ministry of Economy and Competitiveness, `Centro de Excelencia Severo Ochoa 2013-2017', SEV-2012-0208.ca_ES
dc.language.isoengca_ES
dc.publisherNatureca_ES
dc.relationMINECO/PN 2013-2016/BFU2013-50245-EXPca_ES
dc.relationMICINN/PN2008-2011/BFU2012-37162ca_ES
dc.relationMICINN/PN2008-2011/BFU2009-08213ca_ES
dc.relationMICINN/PN2008-2011/BFU2011-30185ca_ES
dc.relationMINECO/PN 2013-2016/BFU2015-71308ca_ES
dc.relationMICINN/PN2008-2011/CDS2009-00016ca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.1038/ncb3343ca_ES
dc.relation.ispartofNature Cell Biology, 2016, vol. 18, núm. 5, p. 516–526ca_ES
dc.rights(c) Macmillan Publishers Limited, 2016ca_ES
dc.subjectCell divisionca_ES
dc.subjectCheckpointsca_ES
dc.subjectCytokinesisca_ES
dc.subjectDNA damage and repairca_ES
dc.titleThe Aurora-B-dependent NoCut checkpoint prevents damage of anaphase bridges after DNA replication stressca_ES
dc.typearticleca_ES
dc.identifier.idgrec024423
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccessca_ES
dc.identifier.doihttps://doi.org/10.1038/ncb3343
dc.date.embargoEndDate2025-01-01


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