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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Gene Review: 

sek-1  -  Protein SEK-1

Caenorhabditis elegans

 
 
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Disease relevance of sek-1

  • A genetic screen for Caenorhabditis elegans mutants with enhanced susceptibility to killing by Pseudomonas aeruginosa led to the identification of two genes required for pathogen resistance: sek-1, which encodes a mitogen-activated protein (MAP) kinase kinase, and nsy-1, which encodes a MAP kinase kinase kinase [1].
 

High impact information on sek-1

  • The fact that DAF-16 translocation by oxidative stress is epistatic to sek-1 suggests that oxidative stress mediates regulation of DAF-16 through activating the p38 signal transduction pathway upstream of daf-16 so as to mobilize DAF-16 to the nucleus and activate transcription [2].
  • However, compared to the wild type PA14, PA14exsA did display a reduced rate of killing of C. elegans strain AU1 which harbours a mutation in the sek-1 gene encoding a MAP kinase involved in nematode innate immunity [3].

References

  1. A conserved p38 MAP kinase pathway in Caenorhabditis elegans innate immunity. Kim, D.H., Feinbaum, R., Alloing, G., Emerson, F.E., Garsin, D.A., Inoue, H., Tanaka-Hino, M., Hisamoto, N., Matsumoto, K., Tan, M.W., Ausubel, F.M. Science (2002) [Pubmed]
  2. The p38 signal transduction pathway participates in the oxidative stress-mediated translocation of DAF-16 to Caenorhabditis elegans nuclei. Kondo, M., Yanase, S., Ishii, T., Hartman, P.S., Matsumoto, K., Ishii, N. Mech. Ageing Dev. (2005) [Pubmed]
  3. The Pseudomonas aeruginosa PA14 type III secretion system is expressed but not essential to virulence in the Caenorhabditis elegans-P. aeruginosa pathogenicity model. Wareham, D.W., Papakonstantinopoulou, A., Curtis, M.A. FEMS Microbiol. Lett. (2005) [Pubmed]
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