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Protection of C. elegans from anoxia by HYL-2 ceramide synthase.

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  • 2009-04-18
Published in:
  • Science (New York, N.Y.). - 2009
Animals
Apoptosis
Caenorhabditis elegans
Caenorhabditis elegans Proteins
Cell Hypoxia
Ceramides
Gene Deletion
Genes, Helminth
Mutation
Oxidoreductases
Oxygen
Receptor, Insulin
Saccharomyces cerevisiae
Sphingomyelins
Substrate Specificity
Transformation, Genetic
Transgenes
English Oxygen deprivation is rapidly deleterious for most organisms. However, Caenorhabditis elegans has developed the ability to survive anoxia for at least 48 hours. Mutations in the DAF-2/DAF-16 insulin-like signaling pathway promote such survival. We describe a pathway involving the HYL-2 ceramide synthase that acts independently of DAF-2. Loss of the ceramide synthase gene hyl-2 results in increased sensitivity of C. elegans to anoxia. C. elegans has two ceramide synthases, hyl-1 and hyl-2, that participate in ceramide biogenesis and affect its ability to survive anoxic conditions. In contrast to hyl-2(lf) mutants, hyl-1(lf) mutants are more resistant to anoxia than normal animals. HYL-1 and HYL-2 have complementary specificities for fatty acyl chains. These data indicate that specific ceramides produced by HYL-2 confer resistance to anoxia.
Language
  • English
Open access status
green
Identifiers
Persistent URL
https://sonar.ch/global/documents/245667
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