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dc.contributor.authorSundaram, Venkatraghavan
dc.contributor.authorIvanova Petkova, Mima
dc.contributor.authorPujol Carrión, Núria
dc.contributor.authorBoada Pallàs, Jordi
dc.contributor.authorTorre Ruiz, M. A. de la
dc.date.accessioned2015-12-12T11:02:18Z
dc.date.issued2015-07-22
dc.identifier.issn0950-382X
dc.identifier.urihttp://hdl.handle.net/10459.1/49261
dc.description.abstractHere we show that Mtl1, member of the cell wall integrity pathway of Saccharomyces cerevisiae, plays a positive role in chronological life span (CLS). The absence of Mtl1 shortens CLS and causes impairment in the mitochondrial function. This is reflected in a descent in oxygen consumption during the postdiauxic state, an increase in the uncoupled respiration and mitochondrial membrane potential and also a descent in aconitase activity. We demonstrate that all these effects are a consequence of signalling defects suppressed by TOR1 (target of rapamycin) and SCH9 deletion and less efficiently by Protein kinase A (PKA)inactivation. Mtl1 also plays a role in the regulation of both Bcy1 stability and phosphorylation, mainly in response to glucose depletion. In postdiauxic phase and in conditions of glucose depletion, Mtl1 negatively regulates TOR1 function leading to Sch9 inactivation and Bcy1 phosphorylation converging in PKA inhibition. Slt2/Mpk1 kinase partially contributes to Bcy1 phosphorylation, although additional targets are not excluded. Mtl1 links mitochondrial dysfunction with TOR and PKA pathways in quiescence, glucose being the main signalling molecule.
dc.description.sponsorshipThis work was supported by the Spanish Ministerio de Economia y Competitividad through Grant BFU2012-31407
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.publisherJohn Wiley & Sons
dc.relationMICINN/PN2008-2011/BFU2012-31407
dc.relation.isformatofReproducció del document publicat a: https://doi.org/10.1111/mmi.13013
dc.relation.ispartofMolecular Microbiology, 2015, vol. 97, num. 1, p. 93-109
dc.rights(c) John Wiley & Sons, 2015
dc.subjectSaccharomyces cerevisiae
dc.subjectPKA
dc.subjectMtl1
dc.subjectMitochondria
dc.subject.classificationMitocondris
dc.subject.classificationSaccharomyces cerevisiae
dc.subject.otherMitochondria
dc.subject.otherSaccharomyces cerevisiae
dc.titleTor1, Sch9 and PKA downregulation in quiescence rely on Mtl1 to preserve mitochondrial integrity and cell survival
dc.typeinfo:eu-repo/semantics/article
dc.date.updated2015-12-12T11:02:19Z
dc.identifier.idgrec023566
dc.type.versioninfo:eu-repo/semantics/publishedVersion
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccess
dc.identifier.doihttps://doi.org/10.1111/mmi.13013
dc.date.embargoEndDate2025-01-01


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