lin-1 encodes an ETS domain transcription factor that functions downstream of a Ras/MAP kinase pathway mediating induction of the 1 degrees cell fate during vulval development in the C. elegans hermaphrodite. Mutants lacking
lin-1 activity display a phenotype similar to that caused by mutations that constitutively activate
let-60 Ras consistent with a model in which
lin-1 is a repressor of the 1 degrees fate whose activity is inhibited by phosphorylation by MPK-1 MAP kinase. Here, we show that, contrary the current model,
lin-1 is required positively for the proper expression of several genes regulated by the pathway in cells adopting the 1 degrees cell fate. We show that the positive requirement for
lin-1 is downstream of
let-60 Ras and
mpk-1 MAP kinase, and that it has a focus in the vulval precursor cells themselves.
lin-1 alleles encoding proteins lacking a docking site for MPK-1 MAP kinase are defective in the positive function. We also show that
lin-1 apparently has both positive and negative functions during the specification of the fates of other cells in the worm requiring Ras/MAP kinase signaling.