Phillips, Aileen

We recently discovered that autophagy, a conserved lysosomal degradation pathway, is necessary for increased lifespan and dauer morphogenesis of daf-2 mutant Caenorhabditis elegans. daf-2 encodes the worm orthologue of an insulin-like growth factor receptor. Moreover, we found neuronal autophagy activity is sufficient to fulfill this requirement. In this study we used the unc-42 promoter to express autophagy gene atg-18 in a subset of C. elegans neurons to examine whether autophagy activity in these neurons is sufficient to execute its function in extension of lifespan and completion of dauer morphogenesis in daf-2 mutants. Here we show expression of atg-18 in these ons fails to rescue the effect of atg-18 mutations on the longevity and dauer morphogenesis of daf-2 mutant worms, indicating that the requirement of neuronal autophagy in C. elegans for these effects is specific to neurons where unc-42 promoter is not active.