PMID:8299935

Citation	Wu, Y and Han, M (1994) Suppression of activated Let-60 ras protein defines a role of Caenorhabditis elegans Sur-1 MAP kinase in vulval differentiation. Genes Dev. 8:147-59
Abstract	The let-60 ras gene of Caenorhabditis elegans is one of the key players in a signal transduction pathway that controls the choice between vulval and epidermal differentiation in response to extracellular signals. To identify components acting downstream of let-60 ras in the vulval signaling pathway, we have identified a reduction-of-function mutation in the sur-1 gene that completely suppresses the multivulva phenotype of a hyperactive let-60 ras mutation. About 10% of animals homozygous for the sur-1 mutation also display a specific and intriguing vulval cell lineage defect. In addition, the sur-1 mutation results in a cold-sensitive egg-laying defective phenotype and a partial larval lethal phenotype. We have cloned the sur-1 gene by DNA-mediated transformation and have shown that it encodes a protein similar in overall structure to mammalian MAP kinases (ERKs). The functional homology between Sur-1 MAP kinase and mammalian MAP kinases was also demonstrated by the ability of a rat ERK2 kinase to rescue the sur-1 mutant phenotypes. Genetic double-mutant analyses place sur-1 downstream of let-60 ras but upstream of lin-1 in the vulval signaling pathway. Our results provide further evidence for the extreme conservation of Ras-mediated signaling pathway between worms and humans and for the function of MAP kinases in cell signaling processes that control cell differentiation and animal development.
Links	PubMed
Keywords	ATP-Binding Cassette Transporters; Amino Acid Sequence; Animals; Base Sequence; Caenorhabditis elegans/embryology; Caenorhabditis elegans/enzymology; Caenorhabditis elegans/genetics; Caenorhabditis elegans Proteins; Cell Differentiation/genetics; Cloning, Molecular; DNA, Complementary; Embryonic Induction/genetics; Female; Genes, ras; Helminth Proteins/genetics; Helminth Proteins/metabolism; Humans; Mitogen-Activated Protein Kinase 1; Molecular Sequence Data; Multidrug Resistance-Associated Proteins; Phenotype; Potassium Channels, Inwardly Rectifying; Protein-Serine-Threonine Kinases/genetics; Protein-Serine-Threonine Kinases/metabolism; Protein-Tyrosine Kinases/genetics; Protein-Tyrosine Kinases/metabolism; Receptors, Drug; Sequence Homology, Amino Acid; Signal Transduction; Suppression, Genetic; Vulva/cytology; ras Proteins
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