Journal
AUTOPHAGY
Volume 4, Issue 7, Pages 870-873Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.6730
Keywords
aging; Beclin 1; Caenorhabditis elegans; nematode; senescence
Categories
Funding
- NIH National Center for Research Resources (NCRR)
- EU 6th Framework Program
- EU 7th Framework Program,
- Ligue contre le Cancer, Agence Nationale pour la Recherche and Institut National sur le Cancer
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The tumor suppressor protein p53 has a major impact on organismal aging. Recently it has become clear that p53 not only controls DNA damage responses, senescence and apoptosis but also plays a major role in the control of autophagy. Thus, deletion, depletion, or inhibition of p53 induces autophagy in human, mouse and nematode cells. We therefore tested the hypothesis that the mutation of the p53 orthologue CEP-1 might increase the life span of Caenorhabditis elegans through an increase in baseline autophagy. For this, we evaluated the survival of nematodes lacking cep-1, alone or in combination with RNA inference with the autophagy gene bec-1 (which encodes the orthologue of Atg6/Beclin 1). cep-1 mutants exhibited a prolonged life span. While BEC-1 depletion (luring adult life did not cause significant modification of the life expectancy of wild type controls, it did reduce the increased life span of cep-1 mutants down to approximately normal levels. These results indicate that the life span-extending effect of the cep-1 mutation is mediated by autophagy. These results lend support to the hypothesis that autophagy has a broad positive impact on organismal aging.
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