During vulval development in the Caenorhabditis elegans hermaphrodite,
the fates of six vulval precursor cells (VPCs) are influenced by dist
inct cell signaling events. In one event, a somatic gonadal cell, the
anchor cell, induces the three nearest VPCs to adopt vulval cell fates
. In another event, lateral signaling between adjacent VPCs specifies
one of two different vulval fates, 1 degrees and 2 degrees. Induction
of vulval fates by the anchor cell is mediated by a signal transductio
n pathway involving let-60 Ras, lin-45 Raf, and mpk-1/sur-1 MAP kinase
, whereas lateral signaling is mediated by lin-12. We have shown that
the mutant phenotype of lin-25, a gene required for VPC fate specifica
tion, results from a defect in vulval induction. Genetic epistasis exp
eriments indicate that lin-25 is required in the inductive signaling p
athway downstream of let-60 Ras and the Raf/MAP kinase cascade. A decr
ease in induction also appears to decrease lateral signaling. We have
cloned and sequenced the lin-25 gene and shown that it encodes a novel
protein that may be a target of the mpk-1/sur-1 MAPK.