We are interested in studying how cells choose their fates. An extremely good system for studying cell fate specification is the development of the hermaphrodite vulva in the soil nematode, Caenorhabditis elegans. In this developmental pathway, vulval precursor cells are induced to adopt vulval cell fates via an EGF receptor/ras/MAP kinase phosphorylation cascade. This study will focus on the identification and characterization of new genes in the cell-signaling pathway responsible for vulval development in C. elegans. While the early stage of this pathway is known to comprise many proteins homologous to those involved in mammalian and Drosophila receptor tyrosine kinase signal transduction, later stages are not well-understood. One of the latest-acting genes in this pathway is the transcription factor, LIN-31 fates (Miller et al., Genes and Dev., 7:933, 1993). To identify genes downstream of the
lin-31 gene, vulvaless (Vul) mutants were isolated in a
lin-31 mutant background (Miller et al, unpublished observations).
lm55 and
lm104, recessive mutations identified in this screen, both enhance the Vul phenotype of a
lin-31 null mutation from 15% Vul to 82% and 85%, respectively..
lm55 has been mapped to a small region of chromosome IV and clearly shows defects in choice of vulval cell fate.
lm104 has been mapped to a small region on the right arm of chromosome II. Both mutations are Vul in the absence of a
lin-31 mutation, indicating that they play a unique and critical role in vulval development.