Journal
JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES
Volume 62, Issue 9, Pages 951-959Publisher
OXFORD UNIV PRESS INC
DOI: 10.1093/gerona/62.9.951
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Funding
- NIAAA NIH HHS [K02 AA 195] Funding Source: Medline
- NIA NIH HHS [R01 AG016219, AG012423] Funding Source: Medline
- NICHD NIH HHS [T32 HD007289] Funding Source: Medline
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Hyperactivation of mammalian p53 has been shown to result in segmental progeria and decreased survivorship. Repression of the p53 homolog in Drosophila melanogaster has also been shown to increase survival. We show that RNA interference (RNAi) or genetic knockout of the Caenorhabditis elegans p53 ortholog, cep-1, leads to increased life span, which is dependent upon functional daf-16. Furthermore, one other DNA damage-responsive C. elegans mutant, hus-1(op241), exhibits a life-span increase. The cep-1(gk138) knockout mutant does not show increased resistance to heat, oxidative, or ultraviolet stress; nor to bacterial pathogenicity. cep-1 RNAi does not extend the life span of a sir-2.1(geln3) overexpressing strain. cep-1 RNAi does not alter dauer formation propensity or nuclear-localization of DAF-16::GFP, even under heat stress; nor does it change nuclear-persistence and/or retention of DAF-16::GFP. This study clarifies the inverse relationship between cep-1 expression and C. elegans life span, and, by extrapolation, that between p53 expression and mammalian life span.
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