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Lifespan extension by calorie restriction relies on the Sty1 MAP kinase stress pathway.
EMBO J. 2010 Mar 03; 29(5):981-91.EJ

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 lifespan extension in fission yeast, and that such effect is dependent on the activation of the stress-dependent Sty1 mitogen-activated protein (MAP) kinase. During transition to stationary phase in glucose-limiting conditions, Sty1 becomes activated and triggers a transcriptional stress programme, 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 lifespan 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 lifespan extension.

Authors+Show Affiliations

Universitat Pompeu Fabra, Barcelona, Spain.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20075862

Citation

Zuin, Alice, et al. "Lifespan Extension By Calorie Restriction Relies On the Sty1 MAP Kinase Stress Pathway." The EMBO Journal, vol. 29, no. 5, 2010, pp. 981-91.
Zuin A, Carmona M, Morales-Ivorra I, et al. Lifespan extension by calorie restriction relies on the Sty1 MAP kinase stress pathway. EMBO J. 2010;29(5):981-91.
Zuin, A., Carmona, M., Morales-Ivorra, I., Gabrielli, N., Vivancos, A. P., Ayté, J., & Hidalgo, E. (2010). Lifespan extension by calorie restriction relies on the Sty1 MAP kinase stress pathway. The EMBO Journal, 29(5), 981-91. https://doi.org/10.1038/emboj.2009.407
Zuin A, et al. Lifespan Extension By Calorie Restriction Relies On the Sty1 MAP Kinase Stress Pathway. EMBO J. 2010 Mar 3;29(5):981-91. PubMed PMID: 20075862.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lifespan extension by calorie restriction relies on the Sty1 MAP kinase stress pathway. AU - Zuin,Alice, AU - Carmona,Mercè, AU - Morales-Ivorra,Isabel, AU - Gabrielli,Natalia, AU - Vivancos,Ana P, AU - Ayté,José, AU - Hidalgo,Elena, Y1 - 2010/01/14/ PY - 2009/11/19/received PY - 2009/12/16/accepted PY - 2010/1/16/entrez PY - 2010/1/16/pubmed PY - 2010/5/12/medline SP - 981 EP - 91 JF - The EMBO journal JO - EMBO J VL - 29 IS - 5 N2 - 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 lifespan extension in fission yeast, and that such effect is dependent on the activation of the stress-dependent Sty1 mitogen-activated protein (MAP) kinase. During transition to stationary phase in glucose-limiting conditions, Sty1 becomes activated and triggers a transcriptional stress programme, 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 lifespan 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 lifespan extension. SN - 1460-2075 UR - https://www.unboundmedicine.com/medline/citation/20075862/Lifespan_extension_by_calorie_restriction_relies_on_the_Sty1_MAP_kinase_stress_pathway_ L2 - https://doi.org/10.1038/emboj.2009.407 DB - PRIME DP - Unbound Medicine ER -