Multiple redundant Wnt signaling components function in two processes during C-elegans vulval development

In Caenorhabditis elegans, vulval precursor cell (VPC) fate is specified by the action of RTK/Ras, Notch and Writ signaling pathways. While the identity of signals for the Ras and Notch pathways is known, the source and identity of the Writ ligand acting on the VPCs are unknown, Single mutations in any of the five Writ 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 Writs are required. Surprisingly, we found that all five Writs 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 Writ function than posterior VPCs, and expression from Wnt::GFP transcriptional reporters showed that the Writs most strongly affecting VPC fate were expressed predominantly in the posterior, suggesting that some of the redundant Writ ligands act over a distance to affect the VPCs. In addition to ligand redundancy, we found that at least three Writ 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 Writ receptors can influence P7.p orientation, suggesting that a surprising amount of functional redundancy exists in Writ signaling during C. elegans vulval induction. (c) 2006 Elsevier Inc. All rights reserved.