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Gene Review

skn-1  -  Protein SKN-1

Caenorhabditis elegans



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High impact information on skn-1

  • SKN-1 is essential for extending lifespan under reduced insulin/IGF-1 signaling conditions that do not induce dauer traits (e.g. daf-2(RNAi) or daf-2 mutants at lower temperatures) [1].
  • SKN-1 is not required for dauer pheromone induced longevity  [1].
  • We propose that the maternally expressed skn-1 gene product acts to specify the fate of the EMS blastomere [2].
  • In skn-1 mutant embryos, EMS instead produces hypodermal cells and body wall muscle cells, much like its sister blastomere [2].
  • SKN-1 is present in ASI nuclei under normal conditions, and accumulates in intestinal nuclei in response to oxidative stress. skn-1 mutants are sensitive to oxidative stress and have shortened lifespans [3].
  • Two genes, skn-1 and pie-1, are required for specifying the different identities of two sister blastomeres in a 4-cell embryo, called P2 and EMS [4].
  • Depletion of skn-1 by RNAi abolishes the expression of all seven reporter transgenes in vivo, confirming that these genes are indeed skn-1 dependent [5].

Biological context of skn-1

  • WT and constitutively nuclear SKN-1 comparably rescue the skn-1 oxidative stress sensitivity, suggesting that an inducible phase II response may provide optimal stress protection [6].
  • The skn-1 gene encodes a DNA binding protein that may control blastomere development by regulating transcription in EMS and its descendants [4].

Other interactions of skn-1

  • We conclude that neither the elt-1 gene nor the skn-1 gene is necessary zygotically for ges-1 expression [7].
  • The sizes of these proteins correspond to the sizes expected for the elt-1 protein and for the skn-1 protein, two regulatory factors present in early C. elegans embryos and possible candidates for ges-1 control [7].


  1. Dauer-independent insulin/IGF-1-signalling implicates collagen remodelling in longevity. Ewald, C.Y., Landis, J.N., Porter Abate, J., Murphy, C.T., Blackwell, T.K. Nature. (2015) [Pubmed]
  2. skn-1, a maternally expressed gene required to specify the fate of ventral blastomeres in the early C. elegans embryo. Bowerman, B., Eaton, B.A., Priess, J.R. Cell (1992) [Pubmed]
  3. SKN-1 links C. elegans mesendodermal specification to a conserved oxidative stress response. An, J.H., Blackwell, T.K. Genes Dev. (2003) [Pubmed]
  4. Determinants of blastomere identity in the early C. elegans embryo. Bowerman, B. Bioessays (1995) [Pubmed]
  5. Identification of lineage-specific zygotic transcripts in early Caenorhabditis elegans embryos. Robertson, S.M., Shetty, P., Lin, R. Dev. Biol. (2004) [Pubmed]
  6. Regulation of the Caenorhabditis elegans oxidative stress defense protein SKN-1 by glycogen synthase kinase-3. An, J.H., Vranas, K., Lucke, M., Inoue, H., Hisamoto, N., Matsumoto, K., Blackwell, T.K. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  7. DNA-protein interactions in the Caenorhabditis elegans embryo: oocyte and embryonic factors that bind to the promoter of the gut-specific ges-1 gene. Stroeher, V.L., Kennedy, B.P., Millen, K.J., Schroeder, D.F., Hawkins, M.G., Goszczynski, B., McGhee, J.D. Dev. Biol. (1994) [Pubmed]
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