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Gene Review

lin-1  -  Protein LIN-1

Caenorhabditis elegans

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High impact information on lin-1

  • We show that MPK-1 directly regulates both the LIN-31 winged-helix and the LIN-1 Ets transcription factors to specify the vulval cell fate. lin-31 and lin-1 act genetically downstream of mpk-1, and both proteins can be directly phosphorylated by MAP kinase [1].
  • The Caenorhabditis elegans gene lin-1 encodes an ETS-domain protein and defines a branch of the vulval induction pathway [2].
  • Genetic double-mutant analyses place sur-1 downstream of let-60 ras but upstream of lin-1 in the vulval signaling pathway [3].
  • Genetic studies showed that mep-1 inhibits vulval cell fates and functions at the level of lin-1 [4].
  • Since expression of egl-17::GFP driven by the distal enhancer can no longer be turned off at late stages in lin-1 and lin-31 mutants, egl-17 may also be regulated by Ras signaling through repression of LIN-1 and LIN-31 activities [5].

Biological context of lin-1

  • Our genetic epistasis experiments suggest that sli-3 functions either downstream or in parallel to nuclear factors lin-1 and sur-2. sli-3 synergistically interacts with the previously identified negative regulators of the let-23 signaling pathway and causes excessive cell proliferation [6].
  • Mutants lacking lin-1 activity display a phenotype similar to that caused by mutations that constitutively activate let-60 Ras consistent with a model in which lin-1 is a repressor of the 1 degree fate whose activity is inhibited by phosphorylation by MPK-1 MAP kinase [7].
  • We show that lin-1 is a negative regulator of vulval cell fates and encodes an ETS-domain putative transcription factor containing potential MAPK phosphorylation sites [2].
  • These missense mutations can be arranged in an allelic series; the strongest mutations eliminate most or all lin-1 functions, and the weakest mutation partially reduces lin-1 function [8].
  • 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 [9].

Associations of lin-1 with chemical compounds

  • We show here that two farnesyltransferase inhibitors, manumycin and gliotoxin, suppress the Multivulva phenotype resulting from an activated let-60 ras mutation, but not the Multivulva phenotype resulting from mutations in the lin-1 gene or the lin-15 gene, which act downstream and upstream of let-60 ras, respectively, in the signaling pathway [10].

Other interactions of lin-1

  • lin-1 encodes an ETS domain transcription factor that functions downstream of a Ras/MAP kinase pathway mediating induction of the 1 degrees cell fate during vulval development in the C. elegans hermaphrodite [7].


  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. The Caenorhabditis elegans gene lin-1 encodes an ETS-domain protein and defines a branch of the vulval induction pathway. Beitel, G.J., Tuck, S., Greenwald, I., Horvitz, H.R. Genes Dev. (1995) [Pubmed]
  3. 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]
  4. Sumoylation of LIN-1 promotes transcriptional repression and inhibition of vulval cell fates. Leight, E.R., Glossip, D., Kornfeld, K. Development (2005) [Pubmed]
  5. Cis regulatory requirements for vulval cell-specific expression of the Caenorhabditis elegans fibroblast growth factor gene egl-17. Cui, M., Han, M. Dev. Biol. (2003) [Pubmed]
  6. sli-3 Negatively Regulates the LET-23/Epidermal Growth Factor Receptor-Mediated Vulval Induction Pathway in Caenorhabditis elegans. Gupta, B.P., Liu, J., Hwang, B.J., Moghal, N., Sternberg, P.W. Genetics (2006) [Pubmed]
  7. lin-1 has both positive and negative functions in specifying multiple cell fates induced by Ras/MAP kinase signaling in C. elegans. Tiensuu, T., Larsen, M.K., Vernersson, E., Tuck, S. Dev. Biol. (2005) [Pubmed]
  8. Identification of residues of the Caenorhabditis elegans LIN-1 ETS domain that are necessary for DNA binding and regulation of vulval cell fates. Miley, G.R., Fantz, D., Glossip, D., Lu, X., Saito, R.M., Palmer, R.E., Inoue, T., Van Den Heuvel, S., Sternberg, P.W., Kornfeld, K. Genetics (2004) [Pubmed]
  9. 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]
  10. Ras farnesyltransferase inhibitors suppress the phenotype resulting from an activated ras mutation in Caenorhabditis elegans. Hara, M., Han, M. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
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