signaling events (Greenwald, 1997). One event, the induction adopt the 2 ° fate.

and MAP kinase. Previous genetic analysis has suggested Ras/MAP kinase pathway do not affect the pattern ofof vulva fates by the anchor cell (AC), is mediated by a signal transduction pathway involving Ras and MAP kinase. Two targets of this pathway in C. elegans are the transcription factors, LIN-1 and LIN-31 (Jacobs et al., 1998; Tan et al., 1998). It is not known in detail, however, how these proteins function to regulate induction, nor have the other targets of the pathway been identified. The vulva in C. elegans is formed from the descendants of three hypodermal (epidermal) cells, P5.p, P6.p and P7.p (Sulston and Horvitz, 1977). These cells are part of a group of six cells, P3.p-P8.p, named collectively the vulva precursor cells (VPCs). Initially each cell has the potential to adopt one of three different fates, 1°, 2 ° or 3 ° (Fig. 1) (Sulston and White, 1980). In wild-type worms P6.p adopts the 1 ° fate, P5.p and P7.p the 2 ° fate, and P3.p, P4.p and P8.p the 3 ° fate. The fate that each cell adopts is thought to be influenced by three The signal that the AC cell sends to P6.p, LIN-3 (Hill and Sternberg, 1992), appears to function by activating the receptor-type tyrosine kinase, LET-23 (Aroian et al., 1990), and in turn a signal transduction pathway involving Ras (LET