Behavior and Vulval Development

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Science  12 Sep 2003:
Vol. 301, Issue 5639, pp. 1447
DOI: 10.1126/science.301.5639.1447c

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) stimulating a Ras-mitogen-activated protein kinase pathway, as well as the Notch-like pathway and the Wnt pathway, contribute 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 locomotory 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 in worms grown on solid media. Thus, behavioral changes in response to environmental conditions may play a role in cell fate specification. — NG

Development 130, 4553 (2003).

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