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, 1978-
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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