A MAP kinase homolog, mpk-1, is involved in ras-mediated induction of vulval cell fates in Caenorhabditis elegans.
During development of the Caenorhabditis elegans hermaphrodite, the gonadal anchor cell induces nearby Pn.p cells to adopt vulval fates. The response to this signal is mediated by a receptor tyrosine kinase signal transduction pathway that has been remarkably well conserved during metazoan evolution. Because mitogen-activated protein (MAP) kinases are activated by receptor tyrosine kinase pathways in vertebrate cells, we hypothesized that C. elegans MAP kinase homologs may play a role in vulval induction. Two C. elegans MAP kinase genes, mpk-1 and mpk-2 (mpk, MAP kinase), were cloned using degenerate oligonucleotide primers and PCR amplification; in parallel, genes involved in vulval induction were identified by screening for mutations that suppress the vulval defects caused by an activated let-60 ras gene. One such suppressor mutation is an allele of mpk-1. We used a new type of mosaic analysis to show that mpk-1 acts cell autonomously in the Pn.p cells. Our results show that mpk-1 plays an important functional role as an activator in ras-mediated cell signaling in vivo.[1]References
- A MAP kinase homolog, mpk-1, is involved in ras-mediated induction of vulval cell fates in Caenorhabditis elegans. Lackner, M.R., Kornfeld, K., Miller, L.M., Horvitz, H.R., Kim, S.K. Genes Dev. (1994) [Pubmed]
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