MAP KINASE SIGNALING SPECIFICITY MEDIATED BY THE LIN-1 ETS LIN31 WH TRANSCRIPTION FACTOR COMPLEX DURING C-ELEGANS VULVAL INDUCTION/

The let-23 receptor/mpk-1 MAP kinase signaling pathway induces the vul va in C. elegans. We show that MPK-1 directly regulates both the LIN-3 1 winged-helix and the LIN-1 Ets transcription factors to specify the vulval cell fate, lin-31 and lin-1 act genetically downstream of mpk-1 , and both proteins can be directly phosphorylated by MAP kinase. LIN- 31 binds to LIN-1, and the LIN-1/LIN-31 complex inhibits vulval induct ion. Phosphorylation of LIN-31 by MPK-1 disrupts the LIN-1/LIN-31 comp lex, relieving vulval inhibition. Phosphorylated LIN-31 may also act a s a transcriptional activator, promoting vulval cell fates. LIN-31 is a vulval-specific effector of MPK-1, while LIN-1 acts as a general eff ector. The partnership of tissue-specific and general effecters may co nfer specificity onto commonly used signaling pathways, creating disti nct tissue-specific outcomes.