Protein-repair and hormone-signaling pathways specify dauer and adult longevity and dauer development in Caenorhabditis elegans

Kelley L. Banfield, Tara A. Gomez, Wendy Lee, Steven Clarke, Pamela L. Larsen

Research output: Contribution to journalArticle

7 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)798-808
Number of pages11
JournalJournals of Gerontology - Series A Biological Sciences and Medical Sciences
Issue number8
StatePublished - Aug 2008



  • Adult and dauer life span
  • Dauer formation
  • Protein L-isoaspartyl methyltransferase
  • daf-2
  • daf-7

ASJC Scopus subject areas

  • Aging
  • Geriatrics and Gerontology

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