Lifespan extension by calorie restriction relies on the Sty1 MAP kinase stress pathway

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Zuin A, Carmona M, Morales-Ivorra I, Gabrielli N, Vivancos A P, Ayté J, Hidalgo E. Lifespan extension by calorie restriction relies on the Sty1 MAP kinase stress pathway. EMBO Journal. 2010; 29: 981-991. DOI 10.1038/emboj.2009.407
http://hdl.handle.net/10230/16236
To cite or link this document: http://hdl.handle.net/10230/16236
dc.contributor.author Zuin, Alice
dc.contributor.author Carmona, Mercè
dc.contributor.author Morales Ivorra, Isabel
dc.contributor.author Gabrielli, Natalia
dc.contributor.author Vivancos Prellezo, Ana
dc.contributor.author Ayté del Olmo, José
dc.contributor.author Hidalgo Hernando, Elena
dc.contributor.other Universitat Pompeu Fabra
dc.date.accessioned 2012-02-15T10:30:36Z
dc.date.available 2012-02-15T10:30:36Z
dc.date.issued 2010
dc.identifier.citation Zuin A, Carmona M, Morales-Ivorra I, Gabrielli N, Vivancos A P, Ayté J, Hidalgo E. Lifespan extension by calorie restriction relies on the Sty1 MAP kinase stress pathway. EMBO Journal. 2010; 29: 981-991. DOI 10.1038/emboj.2009.407
dc.identifier.issn 0261-4189
dc.identifier.uri http://hdl.handle.net/10230/16236
dc.description.abstract Either calorie restriction, loss of function of the nutrient-dependent PKA or TOR/SCH9 pathways, or activation of stress defences improves longevity in different eukaryotes. However, the molecular links between glucose depletion, nutrient-dependent pathways and stress responses are unknown. Here we show that either calorie restriction or inactivation of nutrient-dependent pathways induces life-span extension in fission yeast, and that such effect is dependent on the activation of the stress-dependent Sty1 MAP kinase. During transition to stationary phase in glucose-limiting conditions, Sty1 becomes activated and triggers a transcriptional stress program, whereas such activation does not occur under glucose-rich conditions. Deletion of the genes coding for the SCH9-homologue Sck2 or the Pka1 kinases, or mutations leading to constitutive activation of the Sty1 stress pathway increase life span under glucose-rich conditions, and importantly such beneficial effects depend ultimately on Sty1. Furthermore, cells lacking Pka1 display enhanced oxygen consumption and Sty1 activation under glucose-rich conditions. We conclude that calorie restriction favours oxidative metabolism, reactive oxygen species production and Sty1 MAP kinase activation, and this stress pathway favours life-span extension.
dc.description.sponsorship This work was supported by Dirección General de Investigación of Spain Grants BFU2006-02610 and BFU2009-06933, and by the Spanish program Consolider-Ingenio 2010 Grant CSD 2007-0020 to E.H.
dc.language.iso eng
dc.publisher Nature Publishing Group
dc.rights © 2010 European Molecular Biology Organization. Rights Managed by Nature Publishing Group.
dc.subject.other Proteïnes quinases
dc.subject.other Cèl·lules -- Envelliment
dc.subject.other Estrès oxidatiu
dc.title Lifespan extension by calorie restriction relies on the Sty1 MAP kinase stress pathway
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.1038/emboj.2009.407
dc.subject.keyword MAP kinase
dc.subject.keyword Aging
dc.subject.keyword Oxidative stress
dc.subject.keyword Protein kinase A
dc.subject.keyword Sty1
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/acceptedVersion


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