In C. elegans hermaphrodites, the vulval precursor cells (VPCs) P3.p-P8.p can adopt vulval or hypodermal fates. In wild-type animals, the anchor cell secretes LIN-3, which activates its receptor, LET-23, and causes P5.p-P7.p to adopt vulval fates. Although P3.p, P4.p, and P8.p also express LET-23, it is thought that their distance from the anchor cell prevents levels of activated LET-23 from accumulating necessary to overcome default hypodermal fates. We have used two approaches to study modulation of responses to this inductive signal. In one approach, we tested candidate loci for interaction with this pathway. We find that a loss of function mutation in the egl-15
negative regulator, clr-1
, a receptor tyrosine phosphatase, increases responsiveness of all 6 VPCs to the inductive signal. In contrast, an activated allele of egl-30
Gq alpha facilitates responsiveness of P5.p-P7.p, but not P3.p, P4.p, and P8.p. In a second approach, we identified EMS-induced mutations that enhance the choice of vulval fates by P3.p, P4.p, and P8.p in the presence of a gain-of-function allele of let-23
. Some of these mutations, such as sy622
, strongly enhance the responsiveness of P3.p, P4.p, and P8.p, while only weakly affecting P5.p-P7.p. These results indicate that there are both pan-Pn.p, as well as Pn.p-specific mechanisms operating to modulate vulval induction. Pan-Pn.p mechanisms might function as buffers to lower the overall noise inappropriately contributing to vulval induction. In conjunction with pathways defined by egl-30
(gf) and sy622
which increase responsiveness of P5.p-P7.p and decrease responsiveness of P3.p, P4.p, and P8.p, respectively, a robust response by only a subset of cells might be guaranteed during inductive signaling.