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

Makoto Koga, Yasumi Ohshima

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

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 Dsorl, a Drosophila MAPKK, in each of the three vulvaless mutants lin-3, let-23 and lin-45. The expression of an activated form of Dsorl in each of the mutants effectively induced a normal, functional vulva, that is, suppressed the vulvaless phenotype. The wild type Dsorl also suppressed albeit less effectively. These results suggest that a MAPKK is involved in the vulval induction of C. elegans.

Original languageEnglish
Pages (from-to)15-22
Number of pages8
JournalMechanisms of Development
Volume53
Issue number1
DOIs
Publication statusPublished - Sep 1995

All Science Journal Classification (ASJC) codes

  • Embryology
  • Developmental Biology

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