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dc.contributor.authorPérez Sampietro, María
dc.contributor.authorCasas Herranz, Celia
dc.contributor.authorHerrero Perpiñán, Enrique
dc.date.accessioned2014-05-19T16:10:09Z
dc.date.available2014-05-19T16:10:09Z
dc.date.issued2013
dc.identifier.issn1932-6203
dc.identifier.urihttp://hdl.handle.net/10459.1/47224
dc.description.abstractThe AMPK/Snf1 kinase has a central role in carbon metabolism homeostasis in Saccharomyces cerevisiae. In this study, we show that Snf1 activity, which requires phosphorylation of the Thr210 residue, is needed for protection against selenite toxicity. Such protection involves the Elm1 kinase, which acts upstream of Snf1 to activate it. Basal Snf1 activity is sufficient for the defense against selenite, although Snf1 Thr210 phosphorylation levels become increased at advanced treatment times, probably by inhibition of the Snf1 dephosphorylation function of the Reg1 phosphatase. Contrary to glucose deprivation, Snf1 remains cytosolic during selenite treatment, and the protective function of the kinase does not require its known nuclear effectors. Upon selenite treatment, a null snf1 mutant displays higher levels of oxidized versus reduced glutathione compared to wild type cells, and its hypersensitivity to the agent is rescued by overexpression of the glutathione reductase gene GLR1. In the presence of agents such as diethyl maleate or diamide, which cause alterations in glutathione redox homeostasis by increasing the levels of oxidized glutathione, yeast cells also require Snf1 in an Elm1-dependent manner for growth. These observations demonstrate a role of Snf1 to protect yeast cells in situations where glutathione-dependent redox homeostasis is altered to a more oxidant intracellular environment and associates AMPK to responses against oxidative stress.ca_ES
dc.description.sponsorshipThis work was funded by Ministerio de Economía y Competitividad (Spain) (grants BFU2010-17656 and CSD2007-0020) and Generalitat de Catalunya (grant 2009/SGR/196). MPS is the recipient of a predoctoral fellowship from Generalitat de Catalunya. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
dc.language.isoengca_ES
dc.publisherPublic Library of Scienceca_ES
dc.relationMICINN/PN2008-2011/BFU2010-17656
dc.relationMIECI/PN2004-2007/CSD2007-0020
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.1371/journal.pone.0058283ca_ES
dc.relation.ispartofPLoS ONE, 2013, vol. 8, núm. 3, e58283ca_ES
dc.rightscc-by (c) Pérez-Sampietro et al., 2013
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/es/*
dc.subjectLlevat de cervesaca_ES
dc.subject.otherSaccharomyces cerevisiaeca_ES
dc.subject.otherBiologia molecularca_ES
dc.subject.otherBioquímicaca_ES
dc.titleThe AMPK family member Snf1 protects Saccharomyces cerevisiae cells upon glutatione oxidationca_ES
dc.typearticleca_ES
dc.identifier.idgrec019803
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.identifier.doihttps://doi.org/10.1371/journal.pone.0058283


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