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Asymmetric arginine dimethylation determines life span in C. elegans by regulating forkhead transcription factor DAF-16.

Takahashi Y., Daitoku H., Hirota K., Tamiya H., Yokoyama A., Kako K., Nagashima Y., Nakamura A., Shimada T., Watanabe S., Yamagata K., Yasuda K., Ishii N., Fukamizu A.

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.

Cell Metab. 13:505-516(2011) [PubMed] [Europe PMC]

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