The Caenorhabditis elegans gene mek-2 is required for vulval induction and encodes a protein similar to the protein kinase MEK

Kerry Kornfeld, Kun Liang Guan, H. Robert Horvitz

Research output: Contribution to journalArticle

77 Scopus citations

Abstract

An evolutionarily conserved signal transduction pathway that utilizes a receptor tyrosine kinase and a Ras protein mediates the induction of vulval cell fates in the nematode Caenorhabditis elegans. We sought new genes that function in this pathway by screening for suppressors of the Multivulva phenotype caused by a mutation that activates the let-60 ras gene. Seven such suppressor mutations defined a new gene involved in vulval induction. We named this gene mek-2, because its predicted protein product is most similar to MEK, a protein-serine/threonine and tyrosine kinase. mek-2 mutations can be arranged in an allelic series. A probable null mutation eliminated vulval induction, and the strongest mutations alter codons conserved in most or all protein kinases. Our genetic analysis showed that mek-2 functions downstream of let-60 ras and is required for ras-mediated signal transduction in vivo. The MEK-2 protein may interact with the products of the lin-45 raf and mpk-1 MAP kinase genes, which also mediate vulval induction.

Original languageEnglish
Pages (from-to)756-768
Number of pages13
JournalGenes and Development
Volume9
Issue number6
DOIs
StatePublished - Mar 15 1995
Externally publishedYes

Keywords

  • C. elegans
  • MEK
  • mek 2
  • protein kinase
  • vulval development

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