期刊
CELL REPORTS
卷 14, 期 9, 页码 2059-2067出版社
CELL PRESS
DOI: 10.1016/j.celrep.2016.02.012
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资金
- NIH [P40 OD010440]
- NIH/NIA Ruth L. Kirschstein National Research Service Award [F31 AG039222]
- Glenn/AFAR Postdoctoral Fellow
- NIH/NIA [R01 AG035336, R01 AG038664, R01 AG039756]
- Ellison Medical Foundation Senior Scholar in Aging award
- Glenn Award for Research in Biomedical Mechanisms of Aging from the Glenn Foundation for Medical Research
- NCI [5P30CA030199]
Deficiency of S6 kinase (S6K) extends the lifespan of multiple species, but the underlying mechanisms are unclear. To discover potential effectors of S6K-mediated longevity, we performed a proteomics analysis of long-lived rsks-1/S6K C. elegans mutants compared to wild-type animals. Weidentifiedthe arginine kinaseARGK-1 as the most significantly enriched protein in rsks-1/S6K mutants. ARGK-1 is an ortholog of mammalian creatine kinase, which maintains cellular ATP levels. We found that argk-1 is possibly a selective effector of rsks-1/S6K-mediated longevity and that overexpression of ARGK-1 extends C. elegans lifespan, in part by activating the energy sensor AAK-2/AMPK. argk-1 is also required for the reduced body size and increased stress resistance observed in rsks-1/S6K mutants. Finally, creatine kinase levels are increased in the brains of S6K1 knockout mice. Our study identifies ARGK-1 as a longevity effector in C. elegans with reduced RSKS-1/S6K levels.
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