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 during 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.