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  • Title: A MAP kinase homolog, mpk-1, is involved in ras-mediated induction of vulval cell fates in Caenorhabditis elegans.
    Author: Lackner MR, Kornfeld K, Miller LM, Horvitz HR, Kim SK.
    Journal: Genes Dev; 1994 Jan; 8(2):160-73. PubMed ID: 8299936.
    Abstract:
    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.
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