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Gene Review

mpk-1  -  Protein MPK-1

Caenorhabditis elegans

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High impact information on mpk-1

  • The let-23 receptor/mpk-1 MAP kinase signaling pathway induces the vulva in C. elegans [1].
  • Second, we found that let-23 EGFR prevents vulval induction in a cell-nonautonomous manner, in addition to its cell-autonomous role in activating the let-60 ras/mpk-1 signaling pathway [2].
  • We have cloned and sequenced the lin-25 gene and shown that it encodes a novel protein that may be a target of the mpk-1/sur-1 MAPK [3].
  • 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 [4].
  • 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 [5].

Biological context of mpk-1

  • One such suppressor mutation is an allele of mpk-1 [5].
  • We show that mutations that eliminate mpk-1 activity result in a highly penetrant, vulvaless phenotype [6].
  • Because mpk-1 ERK MAP kinase controls at least one cell-fate decision that does not require lin-1, our results suggest that MPK-1 contributes to the specificity of this receptor tyrosine kinase-Ras-MAP kinase signal transduction pathway by phosphorylating different proteins in different developmental contexts [7].
  • A unique allele of mpk-1, ga111, displays a reversible, temperature-sensitive, tissue-specific defect in progression through meiotic prophase I [8].
  • About 10% of animals homozygous for the sur-1 mutation also display a specific and intriguing vulval cell lineage defect [9].

Anatomical context of mpk-1

  • Moreover, a mosaic analysis of mpk-1, which acts downstream of egl-15, suggests that its suppression of Clr (Soc) function is required in the hypodermis [10].

Regulatory relationships of mpk-1

  • 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 [9].
  • Their mutant phenotype and that of mex-5 mutants can be suppressed by reducing Ras/Map kinase signaling [11].

Other interactions of mpk-1

  • Epistasis analysis suggests that mpk-1 acts downstream of mek-2 (encodes a MEK homolog) and upstream of lin-1 (encodes an Ets transcription factor) in the anchor cell signaling pathway [6].
  • Thus, the recruitment of soc-1/Gab1, and its effectors, into the RTK-signaling complex modifies the cellular response by enhancing Ras/Map kinase signaling while inhibiting PI3K and PLCgamma-mediated signaling [12].
  • Furthermore, as well as stimulating Ras/Map kinase signaling, soc-1/Gab1 stimulates a poorly defined signaling pathway that represses class 2 daf-2 phenotypes [12].


  1. MAP kinase signaling specificity mediated by the LIN-1 Ets/LIN-31 WH transcription factor complex during C. elegans vulval induction. Tan, P.B., Lackner, M.R., Kim, S.K. Cell (1998) [Pubmed]
  2. Inhibition of Caenorhabditis elegans vulval induction by gap-1 and by let-23 receptor tyrosine kinase. Hajnal, A., Whitfield, C.W., Kim, S.K. Genes Dev. (1997) [Pubmed]
  3. lin-25, a gene required for vulval induction in Caenorhabditis elegans. Tuck, S., Greenwald, I. Genes Dev. (1995) [Pubmed]
  4. The Caenorhabditis elegans gene mek-2 is required for vulval induction and encodes a protein similar to the protein kinase MEK. Kornfeld, K., Guan, K.L., Horvitz, H.R. Genes Dev. (1995) [Pubmed]
  5. 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]
  6. Genetic analysis of the Caenorhabditis elegans MAP kinase gene mpk-1. Lackner, M.R., Kim, S.K. Genetics (1998) [Pubmed]
  7. Gain-of-function mutations in the Caenorhabditis elegans lin-1 ETS gene identify a C-terminal regulatory domain phosphorylated by ERK MAP kinase. Jacobs, D., Beitel, G.J., Clark, S.G., Horvitz, H.R., Kornfeld, K. Genetics (1998) [Pubmed]
  8. Expression Profiling of MAP Kinase-Mediated Meiotic Progression in Caenorhabditis elegans. Leacock, S.W., Reinke, V. PLoS Genet. (2006) [Pubmed]
  9. Suppression of activated Let-60 ras protein defines a role of Caenorhabditis elegans Sur-1 MAP kinase in vulval differentiation. Wu, Y., Han, M. Genes Dev. (1994) [Pubmed]
  10. FGF signaling functions in the hypodermis to regulate fluid balance in C. elegans. Huang, P., Stern, M.J. Development (2004) [Pubmed]
  11. The C. elegans E2F- and DP-related proteins are required for embryonic asymmetry and negatively regulate Ras/MAPK signaling. Page, B.D., Guedes, S., Waring, D., Priess, J.R. Mol. Cell (2001) [Pubmed]
  12. The adaptor protein soc-1/Gab1 modifies growth factor receptor output in Caenorhabditis elegans. Hopper, N.A. Genetics (2006) [Pubmed]
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