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Lifespan extension by calorie restriction relies on the Sty1 MAP kinase stress pathway
Zuin, Alice; Carmona, Mercè; Morales Ivorra, Isabel; Gabrielli, Natalia; Vivancos Prellezo, Ana; Ayté del Olmo, José; Hidalgo Hernando, Elena
Universitat Pompeu Fabra
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.
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.
02-07-2013
Proteïnes quinases
Cèl·lules -- Envelliment
Estrès oxidatiu
MAP kinase
Aging
Oxidative stress
Protein kinase A
Sty1
© 2010 European Molecular Biology Organization. Rights Managed by Nature Publishing Group.
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