Sir2 histone deacetylase prevents programmed cell death caused by sustained activation of the Hog1 stress-activated protein kinase

Vendrell Arasa, Alexandre; Martínez Pastor, Mar; González Novo, Alberto; Pascual Ahuir, Amparo; Sinclair, David A.; Proft, Markus; Posas Garriga, Francesc

Sir2 histone deacetylase prevents programmed cell death caused by sustained activation of the Hog1 stress-activated protein kinase

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dc.contributor.author Vendrell Arasa, Alexandreca
dc.contributor.author Martínez Pastor, Marca
dc.contributor.author González Novo, Albertoca
dc.contributor.author Pascual Ahuir, Amparoca
dc.contributor.author Sinclair, David A.ca
dc.contributor.author Proft, Markusca
dc.contributor.author Posas Garriga, Francescca
dc.date.accessioned 2015-12-17T16:33:23Z
dc.date.available 2015-12-17T16:33:23Z
dc.date.issued 2011
dc.description.abstract Exposure of yeast to high osmolarity induces a transient activation of the Hog1 stress-activated protein kinase (SAPK), which is required for cell survival under these conditions. However, sustained activation of the SAPK results in a severe growth defect. We found that prolonged SAPK activation leads to cell death, which is not observed in nma111 cells, by causing accumulation of reactive oxygen species (ROS). Mutations of the SCF(CDC4) ubiquitin ligase complex suppress cell death by preventing the degradation of Msn2 and Msn4 transcription factors. Accumulation of Msn2 and Msn4 leads to the induction of PNC1, which is an activator of the Sir2 histone acetylase. Sir2 is involved in protection against Hog1-induced cell death and can suppress Hog1-induced ROS accumulation. Therefore, cell death seems to be dictated by the balance of ROS induced by Hog1 and the protective effect of Sir2.ca
dc.description.sponsorship This work was supported by grants from the Ministerio de Ciència y Innovación (BIO2009-07762) and Consolider Ingenio 2010 programme (grant CSD2007-0015), UNICELLSYS from FP7, as well as supported byFundación Marcelino Botín. F.P. is the recipient of the Institució Catalana de Recerca i Estudis Avançats Acadèmia (Generalitat de Catalunya). D.A.S. is supported by grants from the National Institute on Aging National Institutes of Health, the Ellison Medical Foundation and the Glenn Foundation for Medical Research.
dc.format.mimetype application/pdfca
dc.identifier.citation Vendrell A, Martínez-Pastor M, González-Novo A, Pascual-Ahuir A, Sinclair DA, Proft M et al. Sir2 histone deacetylase prevents programmed cell death caused by sustained activation of the Hog1 stress-activated protein kinase. EMBO reports. 2011;12(10):1062-608. DOI 10.1038/embor.2011.154ca
dc.identifier.doi http://dx.doi.org/10.1038/embor.2011.154
dc.identifier.issn 1469-221X
dc.identifier.uri http://hdl.handle.net/10230/25460
dc.language.iso engca
dc.publisher Nature Publishing Groupca
dc.relation.ispartof EMBO reports. 2011;12(10):1062-608
dc.relation.projectID info:eu-repo/grantAgreement/ES/3PN/BIO2009-07762
dc.rights.accessRights info:eu-repo/semantics/openAccessca
dc.rights.uri http://creativecommons.org/licenses/by-nc-sa/3.0/ca
dc.subject.other Saccharomyces cerevisiae -- Metabolismeca
dc.subject.other Factors de transcripcióca
dc.subject.other Proteïnesca
dc.title Sir2 histone deacetylase prevents programmed cell death caused by sustained activation of the Hog1 stress-activated protein kinaseca
dc.type info:eu-repo/semantics/articleca
dc.type.version info:eu-repo/semantics/publishedVersionca

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