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dc.contributor.authorPetkova, Mima Ivanova
dc.contributor.authorPujol Carrión, Núria
dc.contributor.authorArroyo, Javier
dc.contributor.authorGarcia-Cantalejo, J.
dc.contributor.authorTorre Ruiz, M. A. de la
dc.date.accessioned2017-02-22T09:30:01Z
dc.date.available2017-02-22T09:30:01Z
dc.date.issued2010
dc.identifier.issn0021-9258
dc.identifier.urihttp://hdl.handle.net/10459.1/59299
dc.description.abstractMtl1 is a member of the cell wall integrity (CWI) pathway of Saccharomyces cerevisiae, which functions as a cell wall sensor for oxidative stress. Genome-wide transcriptional analysis revealed a cluster of genes that were down-regulated in the absence of Mtl1. Many of these genes were potentially regulated by the general stress response factor Msn2/Msn4. In response to rapamycin, caffeine, glucose starvation and oxidative stress provoked by H(2)O(2), mtl1 presents a significant loss of viability as well as a deficiency in the transcriptional response mediated by Msn2/Msn4. The Mtl1 function was required (i) to induce ribosomal gene repression, (ii) to induce the general stress response driven by the transcription factor Msn2/Msn4, and (iii) to activate the CWI pathway in response to both glucose starvation and oxidative stress. We also detected higher cAMP levels in the mtl1 mutant than in wild type cells indicative of up-regulated RAS2-PKA activity. Disruption of TOR1, disruption of RAS2, or hyperactivation of Rho1 restored both the viability and the transcriptional function (both ribosomal and Msn2/Msn4-dependent gene expression) in the mtl1 mutant to almost wild type levels when cells were starved of glucose or stressed with H(2)O(2). Taking our results together, we propose an essential role for Mtl1 in signaling oxidative stress and quiescence to the CWI pathway and to the general stress response through Rho1 and the inhibition of either the TOR1 or RAS2 functions. These mechanisms would be required to allow cells to adapt to both oxidative and nutritional stresses.ca_ES
dc.description.sponsorshipThis work was supported by Ministerio de Educacion y Ciencia (Spanish government) Grants BFU2009-11215 and BIO2007-67821 and Comunidad de Madrid (Spain) Grant S-SAL-0246/2006.ca_ES
dc.language.isoengca_ES
dc.publisherAmerican Society for Biochemistry and Molecular Biologyca_ES
dc.relationMICINN/PN2008-2011/BFU2009-11215ca_ES
dc.relationMIECI/PN2004-2007/BIO2007-67821ca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.1074/jbc.M109.085282ca_ES
dc.relation.ispartofJournal of Biological Chemistry, 2010, vol. 285, núm. 25, p. 19521-19531ca_ES
dc.rights(c) American Society for Biochemistry and Molecular Biology, 2010ca_ES
dc.subject.otherEstrès oxidatiuca_ES
dc.titleMtl1 is required to activate general stress response through Tor1 and Ras2 inhibition under conditions of glucose starvation and oxidative stressca_ES
dc.typearticleca_ES
dc.identifier.idgrec019574
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.identifier.doihttps://doi.org/10.1074/jbc.M109.085282


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