Insulin htts on Autophagy

Macroautophagocytosis has been shown to participate in the degradation and clearance of polyglutamine (polyQ) tract-containing proteins generated by trinucleotide repeat expansion mutations. Large expansions are the genetic cause of diseases such as Huntington’s disease that lead to neuronal dysfunction due to polyQ protein aggregates. Recently, a functional screen performed by Yamamoto et al. to investigate proteins that regulate such autophagic processes revealed a novel role for insulin signaling in the promotion of autophagy of mutant protein aggregates. This suggests that insulin/insulin-like growth factor signaling pathways not only prevent the induction of autophagy, but paradoxically may promote autophagy of deleterious proteins in certain circumstances.

Commentary to:

Autophagy-Mediated Clearance of Huntingtin Aggregates Triggered by the Insulin-Signaling Pathway

A. Yamamoto, M.L. Cremona and J.E. Rothman

J Cell Biol 2006; 172:719-31