Fleeing Overexposure

Abstract

Locomotion in the nematode Caenorhabditis elegans depends on neuronal Gα q and Gα s signaling pathways involved in synaptic function. Thus, worms in which either of these signaling pathways are nonfunctional are virtually paralyzed. Edwards et al . found that exposure to blue-violet light restored coordinated locomotion to worms with loss-of-function mutations affecting either Gα q or Gα s signaling pathways. Only short-wavelength light was effective in eliciting locomotion, through a mechanism that did not depend on temperature change, with the maximal response occurring with exposure to ultraviolet light. Prolonged exposure to short-wavelength light was lethal, and, given the option, wild-type worms avoided short-wavelength illumination. A forward genetic screen for motile worms that lacked a locomotive response to short-wavelength light implicated a protein that the authors called LITE-1. Intriguingly, LITE-1 is unrelated to any known photoreceptor protein but instead resembles an insect Gustatory receptor (Gr) protein. When lite-1 was expressed in the neurons of lite-1 -null mutant worms, it restored light-induced locomotion; when heterologously expressed in body wall and egg-laying muscles, it elicited light-induced contraction and egg expulsion. Thus, the authors conclude that LITE-1 represents a photoreceptor for ultraviolet light that may allow C. elegans to avoid lethal exposure to sunlight. S. L. Edwards, N. K. Charlie, M. C. Milfort, B. S. Brown, C. N. Gravlin, J. E. Knecht, K. G. Miller, A novel molecular solution for ultraviolet light detection in Caenorhabditis elegans . PLoS Biol. 6 , e198 (2008). [PubMed]