In Caenorhabditis elegans, vulval precursor cell (VPC) fate is specified by the action of RTK/Ras, Notch and Wnt signaling pathways. While the identity of signals for the Ras and Notch pathways is known, the source and identity of the Wnt ligand acting on the VPCs are unknown. Single mutations in any of the five Wnt genes (lin-44, cwn-1, cwn-2, egl-20 and mom-2) do not cause strong defects in VPC fate specification, suggesting that functionally redundant Wnts are required. Surprisingly, we found that all five Wnts influence VPC fate. The strongest defects we observed were in the lin-44; cwn-1; egl-20 triple mutant. Anterior VPCs were more strongly affected by loss of Wnt function than posterior VPCs, and expression from WntColon, two colonsGFP transcriptional reporters showed that the Wnts most strongly affecting VPC fate were expressed predominantly in the posterior, suggesting that some of the redundant Wnt ligands act over a distance to affect the VPCs. In addition to ligand redundancy, we found that at least three Wnt receptors, lin-17, mom-5 and mig-1, function in the VPCs. We also examined ligand and receptor function in another Wnt-mediated vulval process, the orientation of the P7.p lineage. Here, too, we found that four of five Wnt receptors can influence P7.p orientation, suggesting that a surprising amount of functional redundancy exists in Wnt signaling during C. elegans vulval induction.