Ultraviolet B acts as a dietary restriction mimetic by targeting mitochondrial bioenergetics.

Abstract

Ultraviolet (UV) light is a common environmental stimulus, and UV exposure confers health benefits, with cellular targets still unclear. Here, we show that ultraviolet B (UVB) exposure alters mitochondrial bioenergetics in C. elegans and human skin fibroblasts triggering loss of membrane potential, mitochondrial fission and calcium release. This initial stress is followed by a recovery process relying on mitochondrial biogenesis and fusion, which prevents lasting mitochondrial damage. Strikingly, the transient decline of ATP synthesis caused by UVB-induced mitochondrial changes triggers a swift metabolic re-wiring response that resembles effects of dietary restriction (DR) at the organismal and molecular levels. Both recovery from UVB and DR-mimetic UVB effects require mitochondrial fusion, and we found that dysfunction of fusion during aging abrogates UVB benefits and sensitizes old nematodes to UVB toxicity. Finally, UVB irradiation of the skin was effective in inducing organismal fasting-like phenomena in proof-of-concept tests in young mice. We thus uncovered a novel evolutionary conserved cellular mechanism connecting UV light and metabolism. Our findings illuminate potential DR-mimetic properties of UVB and explain late life-specific UVB intolerance.