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].

References