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dc.contributor.authorClotet Bellmunt, Josep
dc.contributor.authorEscoté, Xavier
dc.contributor.authorÀngel Adrover, Miquel
dc.contributor.authorYaakov, Gilad
dc.contributor.authorGarí Marsol, Eloi
dc.contributor.authorAldea, Martí
dc.contributor.authorde Nadal, Eulàlia
dc.contributor.authorPosas, Francesc
dc.date.accessioned2017-01-20T08:00:22Z
dc.date.issued2006
dc.identifier.issn0261-4189
dc.identifier.urihttp://hdl.handle.net/10459.1/59047
dc.description.abstractControl of cell cycle progression by stress-activated protein kinases (SAPKs) is essential for cell adaptation to extracellular stimuli. Exposure of yeast to osmostress leads to activation of the Hog1 SAPK, which controls cell cycle at G1 by the targeting of Sic1. Here, we show that survival to osmostress also requires regulation of G2 progression. Activated Hog1 interacts and directly phosphorylates a residue within the Hsl7-docking site of the Hsl1 checkpoint kinase, which results in delocalization of Hsl7 from the septin ring and leads to Swe1 accumulation. Upon Hog1 activation, cells containing a nonphosphorylatable Hsl1 by Hog1 are unable to promote Hsl7 delocalization, fail to arrest at G2 and become sensitive to osmostress. Together, we present a novel mechanism that regulates the Hsl1–Hsl7 complex to integrate stress signals to mediate cell cycle arrest and, demonstrate that a single MAPK coordinately modulates different cell cycle checkpoints to improve cell survival upon stress.ca_ES
dc.description.sponsorshipWe thank Y Barral, J Ayté, E Herrero, S Moreno, M Winey, A Casamayor, G Gil and G Ammerer for valuable advice, plasmids and strains; O` scar Fornas, Laia Subirana and Marisa Rodriguez for their excellent technical assistance. XE was recipient of an FPI fellowship (MEC, Spanish Government) and MA Adrover is recipient of an FPU fellowship (MEC). We declare that we have no financial conflict of interest. This work was supported by grants from Ministerio de Ciencia y Tecnologı´a (BMC2003-00321), ‘Distincio´ de la Generalitat de Catalunya per a la Promocio´ de la Recerca Universitaria, Joves Investigadors’ DURSI (Generalitat de Catalunya) and the EURYI program (ESF) to FP.ca_ES
dc.language.isoengca_ES
dc.publisherEMBOPressca_ES
dc.relationMICYT/PN2000-2003/BMC2003-00321ca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.1038/sj.emboj.7601095ca_ES
dc.relation.ispartofThe EMBO Journal, 2006, vol. 25, p. 2338–2346ca_ES
dc.rights(c) European Molecular Biology Organization, 2006ca_ES
dc.subjectCell cycleca_ES
dc.subjectHog1ca_ES
dc.subjectHsl1ca_ES
dc.subjectOsmostressca_ES
dc.subjectSAPKca_ES
dc.titlePhosphorylation of Hsl1 by Hog1 leads to a G2 arrest essential for cell survival at high osmolarityca_ES
dc.typearticleca_ES
dc.identifier.idgrec010681
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccessca_ES
dc.identifier.doihttps://doi.org/10.1038/sj.emboj.7601095
dc.date.embargoEndDate2025-01-01


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