Development of the vulva of the nematode Caenorhabditis elegans is a model for studying cell fate signaling. The epidermal growth factor receptor-like tyrosine kinase (LET-23), which stimulates a Ras-mitogen-activated protein kinase pathway, as well as the Notch-like pathway and the Wnt pathway, contributes to vulval development. A gain-of-function mutant of the Gαq homolog, EGL-30, exhibited rare ectopic vulval tissue. These worms also exhibit hyperactive locomotor and egg-laying behaviors. Moghal et al. used genetic interactions and targeted gene expression to show that EGL-30 expressed in motor neurons promoted vulval induction. The ability of EGL-30 to promote vulval development required the L-type voltage-gated calcium channel (EGL-19) expressed in body wall muscles. EGL-30 did not appear to be acting through the LET-23 pathway; however, EGL-30 vulval development was inhibited by loss of β-catenin (BAR-1) of the Wnt pathway. Consistent with behavior modulating vulval development, loss-of-function mutations in egl-30 did not affect vulval development of worms grown on solid media, but did inhibit vulval development of worms grown in liquid culture. In liquid, the worms exhibit a dramatically more vigorous movement than that observed for worms grown on solid media. Thus, the authors propose that behavior changes in response to environmental conditions appear to play a role in cell fate specification.
N. Moghal, L. R. Garcia, L. A. Khan, K. Iwasaki, P. W. Sternberg, Modulation of EGF receptor-mediated vulva development by the heterotrimeric G-protein Gq and excitable cells in C. elegans. Development 130, 4553-4566 (2003). [Abstract] [Full Text]