A radical role for TOR in longevity

Abstract

TOR (target of rapamycin) signaling regulates life span in many organisms, but the mechanism behind the effect is unknown. In this issue of Cell Metabolism, Pan and colleagues (2011) find that reduced TORC1 activity promotes yeast life span via a mechanism that, paradoxically, relies upon the production of normally deleterious reactive oxygen species.

Figure 1. Rapamycin promotes yeast chronological lifespan

Rapamycin treatment of a yeast culture (top) during the logarithmic growth phase increases mitochondrial respiration and the generation of reactive oxygen species, resulting in the induction of cellular defense mechanisms that protect the yeast and will preserve viability during stationary phase. In contrast, an untreated yeast culture (bottom) experiences less oxidative stress during logarithmic growth, and is unprepared for the harsh environment of stationary phase. Figure by Tom DiCesare, Whitehead Institute.