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1 Department of Chemistry and Biochemistry and the Molecular Biology Institute, University of California, Los Angeles.
2 Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio.
Address correspondence to Pamela L. Larsen, PhD, Department of Cellular and Structural Biology, University of Texas Science Center at San Antonio, San Antonio TX 78229. E-mail: larsenp{at}uthscsa.edu
Protein damage that accumulates during aging can be mitigated by a repair methyltransferase, the L-isoaspartyl-O-methyltransferase. In Caenorhabditis elegans, the pcm-1 gene encodes this enzyme. In response to pheromone, we show that pcm-1 mutants form fewer dauer larvae with reduced survival due to loss of the methyltransferase activity. Mutations in daf-2, an insulin/insulin-like growth factor-1-like receptor, and daf-7, a transforming growth factor-β–like ligand, modulate pcm-1 dauer defects. Additionally, daf-2 and daf-7 mutant dauer larvae live significantly longer than wild type. Although dauer larvae are resistant to many environmental stressors, a proportionately larger decrease in dauer larvae life spans occurred at 25°C compared to 20°C than in adult life span. At 25°C, mutation of the daf-7 or pcm-1 genes does not change adult life span, whereas mutation of the daf-2 gene and overexpression of PCM-1 increases adult life span. Thus, there are both overlapping and distinct mechanisms that specify dauer and adult longevity.
Key Words: Adult and dauer life span • Dauer formation • Protein L-isoaspartyl methyltransferase • daf-2 • daf-7
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