The cellular housekeeping program known as autophagy — which allows the recycling of old (and potentially damaged) proteins, lipids, and even whole organelles — is essential to maintaining cellular health over long periods of time. Recent findings implicate autophagy in the regulation of lifespan: Without autophagy, damaged macromolecules will slowly accumulate over time, potentially resulting in a breakdown of cellular homeostasis termed a garbage catastrophe — and unfortunately, it appears that the efficiency of autophagy decreases with age.

Two recent articles underscore the importance of autophagy in the longevity of two favorite model systems: the fly Drosophila and the worm C. elegans. Juhász and Neufeld report that fly mutants in the autophagy gene Atg7 are viable and develop normally, but are hypersensitive to oxidation and starvation stress (two hallmarks of premature aging mutants) and undergo premature neuronal cell death. These results are consistent with earlier findings linking defects in lysosomal trafficking (the intracellular sorting mechanism that guides the targets of autophagy to their ultimate fate) to shortened longevity, stress resistance and phenotypes of premature aging.

Meanwhile, in the worm (where, autophagy is a two-edged sword, at least in the “brain”) Tóth et al. describe how multiple longevity assurance pathways (IGF-1 and TOR) converge on autophagy. They argue that the regulation of autophagy represents a key mechanism by which these pathways regulate longevity — a model that makes a large number of strong predictions about genetic interactions between these pathways (predictions which, one hopes, the authors are currently hard at work testing).