The synthetic multivulval genes of C. elegans: functional redundancy, Ras-antagonism, and cell fate determination.

Development of the C. elegans vulva requires coordination between a strikingly complex set of molecular regulators and pathways. In particular, the correct specification of vulval cell-fates requires both the activation of RTK/Ras/Map kinase members as well as negative regulation by a set of genes known as the SynMuvs. SynMuvs comprise two functionally redundant sets of genes that appear to antagonize Ras pathway signaling. In this way, SynMuv genes act to limit the number of cells adopting vulval fates. Recently, a number of SynMuv genes have been shown to encode worm homologs of the Rb transcriptional-regulatory complex. These and other results are discussed and we present several models for understanding the role of SynMuv genes in vulval development.