LET-23 RECEPTOR LOCALIZATION BY THE CELL JUNCTION PROTEIN LIN-7 DURING C-ELEGANS VULVAR INDUCTION

In C. elegans, the anchor cell signal induces Pn.p cells to form the v ulva by activating a conserved receptor tyrosine kinase pathway. lin-2 and lin-7 mutants exhibit a vulvaless phenotype similar to the phenot ype observed when this signaling pathway is defective. We have found t hat LIN-7 is a cell junction-associated protein that binds to the LET- 23 receptor tyrosine kinase. LET-23 is also localized to the cell junc tions, and both LIN-2 and LIN-7 are required for this localization. LE T-23 overexpression rescues the lin-2 or lin-7 vulvaless phenotype, su ggesting that increased receptor density can compensate for mislocaliz ation. These results suggest that proper localization of LET-23 recept or to the Pn.p cell junctions is required for signaling activity.