Drosophila MAP kinase kinase suppresses the vulvaless phenotype of lin-3, let-23 and lin-45 mutations in Caenorhabditis elegans.

The vulva of the nematode Caenorhabditis elegans develops from the three vulval precursor cells (VPCs) that are induced by a signal from the gonadal anchor cell. This signal is thought to be mediated by a receptor tyrosine kinase (RTK) in the VPCs to a downstream signal transduction pathway. A mitogen-activated protein kinase kinase (MAPKK) has been found to be one of the major components of an RTK pathway in other organisms. We expressed a wild type and an activated cDNA of Dsor1, a Drosophila MAPKK, in each of the three vulvaless mutants lin-3, let-23 and lin-45. The expression of an activated from of Dsor1 in each of the mutants effectively induced a normal, functional vulva, that is, suppressed the vulvaless phenotype. The wild type Dsor1 also suppressed albeit less effectively. These results suggest that a MAPKK is involved in the vulval induction of C. elegans.