The development of the vulva of the nematode Caenorhabditis elegans isinduced by a signal from the anchor cell of the somatic gonad. Activity of thegene lin-3 is required for the Vulval Precursor Cells (VPCs) to assume vulvalfates. It is shown here that lin-3 encodes the vulval-inducing signal.
lin-3 was molecularly cloned by transposon-tagging and shown to encodea nematode member ofthe Epidermal Growth Factor (EGF) family. Geneticepistasis experiments indicate that lin-3 acts upstream of let-23, whichencodes a homologue of the EGF-Receptor.
lin-3 transgenes that contain multiple copies of wild-type lin-3 genomicDNA clones confer a dominant multivulva phenotype in which up to all six ofthe VPCs assume vulval fates. The properties of these trans genes suggestthat lin-3 can act in the anchor cell to induce vulval fates. Ablation of thegonadal precursors, which prevents the development of the AC, stronglyreduces the ability of lin-3 transgenes to stimulate vulval development. Alin-3 recorder transgene that retains the ability to stimulate vulvaldevelopment is expressed specifically in the anchor cell at the time of vulvalinduction.
Expression of an obligate secreted form of the EGF domain of Lin-S froma heterologous promoter is sufficient to induce vulval fates in the absence ofthe normal source of the inductive signal. This result suggests that Lin-Smay act as a secreted factor, and that Lin-S may be the sole vulval-inducingsignal made by the anchor cell.
lin-3 transgenes can cause adjacent VPCs to assume the 1° vulval fateand thus can override the action of the lateral signal mediated by lin-12 thatnormally prevents adjacent 1° fates. This indicates that the production ofLin-3 by the anchor cell must be limited to allow the VPCs to assume theproper pattern of fates of so 3° 3° 2° 1° 2° 3°.
