期刊
CELL METABOLISM
卷 13, 期 5, 页码 505-516出版社
CELL PRESS
DOI: 10.1016/j.cmet.2011.03.017
关键词
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资金
- Ministry of Education, Culture, Sports, Science, and Technology [17054004, 22688029, 10J00386]
- Grants-in-Aid for Scientific Research [21510222, 23658283, 22688029, 17054004, 22248040, 22590666, 10J00386, 22510064] Funding Source: KAKEN
Arginine methylation is a widespread posttranslational modification of proteins catalyzed by a family of protein arginine methyltransferases (PRMTs). It is well established that PRMTs are implicated in various cellular processes, but their physiological roles remain unclear. Using nematodes with a loss-of-function mutation, we show that prmt-1, the major asymmetric arginine methyltransferase, is a positive regulator of longevity in C. elegans. This regulation is dependent on both its enzymatic activity and DAF-16/FoxO transcription factor, which is negatively regulated by AKT-mediated phosphorylation downstream of the DAF-2/insulin signaling. prmt-1 is also required for stress tolerance and fat storage but not dauer formation in daf-2 mutants. Biochemical analyses indicate that PRMT-1 methylates DAF-16, thereby blocking its phosphorylation by AKT. Disruption of PRMT-1 induces phosphorylation of DAF-16 with a concomitant reduction in the expression of longevity-related genes. Thus, we provide a mechanism by which asymmetric arginine dimethylation acts as an antiaging modification in C. elegans.
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