A bidirectional crosstalk between autophagy and TP53 determines the pace of aging.

Abstract

When the orthologue of tumor suppressor protein p53 (TP53), cep-1, is inactivated in Caenorhabditis elegans, the nematodes manifest an autophagy-dependent increase in lifespan. A recent paper by Yang et al. demonstrates that accelerated aging phenotype of autophagy-deficient mice can be reduced by the knockout (KO) of Trp53. These findings point to a complex bidirectional crosstalk between autophagy and TP53 that has vast implications for the aging process.