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dc.contributor.authorDuch, Albaes_ES
dc.contributor.authorFelipe-Abrio, Irenees_ES
dc.contributor.authorBarroso, Soniaes_ES
dc.contributor.authorYaakov, Gilades_ES
dc.contributor.authorGarcía-Rubio, María L.es_ES
dc.contributor.authorAguilera, Andréses_ES
dc.contributor.authorPosas, Francesces_ES
dc.date.accessioned2015-09-01T10:59:03Z-
dc.date.available2015-09-01T10:59:03Z-
dc.date.issued2012-11-25-
dc.identifier.citationNature 493(7430): 116-119 (2013)es_ES
dc.identifier.issn0028-0836-
dc.identifier.urihttp://hdl.handle.net/10261/121554-
dc.description.abstractUpon environmental changes or extracellular signals, cells are subjected to marked changes in gene expression 1,2. Dealing with high levels of transcription during replication is critical to prevent collisions between the transcription and replication pathways and avoid recombination events3–5. In response to osmostress, hundreds of stress-responsive genes are rapidly induced by the stress-activated protein kinase (SAPK) Hog1 (ref. 6), even during S phase7. Here we show in Saccharomyces cerevisae that a single signalling molecule, Hog1, coordinates both replication and transcription upon osmostress. Hog1 interacts with and phosphorylates Mrc1, a component of the replication complex8–11. Phosphorylation occurs at different sites to those targeted by Mec1 upon DNA damage8,9. Mrc1 phosphorylation by Hog1 delays early and late origin firing by preventing Cdc45 loading, as well as slowing down replication-complex progression. Regulation of Mrc1 by Hog1 is completely independent of Mec1 and Rad53. Cells carrying a non-phosphorylatable allele of MRC1 (mrc13A) do not delay replication upon stress and show a marked increase in transcription-associated recombination, genomic instability and Rad52 foci. In contrast, mrc13A induces Rad53 and survivalin the presence of hydroxyurea or methylmethanesulphonate. Therefore, Hog1 and Mrc1 define a novel S-phase checkpoint independent of the DNA-damage checkpoint that permits eukaryotic cells to prevent conflicts between DNA replication and transcription, which would otherwise lead to genomic instability when both phenomena are temporally coincident.es_ES
dc.description.sponsorshipThis work was supported by grants from the Spanish Government (BIO2009-07762 and BFU2012-33503 to F.P., BFU2011-26722 to E.d.N., BFU2010- 16372 to A.A., and Consolider Ingenio 2010 programme CSD2007-0015 to F.P. and A.A.) and FP7 UNICELLSYS grant (no. 201142) and the Fundación Marcelino Botín to F.P. F.P. and E.d.N. are recipients of an ICREA Acadèmia (Generalitat de Catalunya).es_ES
dc.language.isoenges_ES
dc.publisherNature Publishing Groupes_ES
dc.relationinfo:eu-repo/grantAgreement/EC/FP7/201142es_ES
dc.rightsclosedAccesses_ES
dc.subjectDNA damage checkpointses_ES
dc.subjectDNA replicationes_ES
dc.subjectTranscriptiones_ES
dc.subjectCell biologyes_ES
dc.titleCoordinated control of replication and transcription by a SAPK protects genomic integrityes_ES
dc.typeartículoes_ES
dc.identifier.doi10.1038/nature11675-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttp://dx.doi.org/10.1038/nature11675es_ES
dc.identifier.e-issn1476-4687-
dc.contributor.funderMinisterio de Economía y Competitividad (España)es_ES
dc.contributor.funderEuropean Commissiones_ES
dc.contributor.funderFundación Botínes_ES
dc.contributor.funderInstitución Catalana de Investigación y Estudios Avanzadoses_ES
dc.contributor.funderGeneralitat de Catalunya-
dc.relation.csices_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003329es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100000780es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100006373es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100003741es_ES
dc.identifier.funderhttp://dx.doi.org/10.13039/501100002809es_ES
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