Abstract
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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis
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Caenorhabditis elegans / cytology
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Caenorhabditis elegans / genetics
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Caenorhabditis elegans / physiology*
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Caenorhabditis elegans Proteins / genetics*
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Caenorhabditis elegans Proteins / metabolism*
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Cell Hypoxia*
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Ceramides / biosynthesis
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Ceramides / physiology*
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Gene Deletion
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Genes, Helminth
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Mutation
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Oxidoreductases / genetics*
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Oxidoreductases / metabolism*
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Oxygen / physiology*
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Receptor, Insulin / genetics
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Receptor, Insulin / metabolism
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Saccharomyces cerevisiae / genetics
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Saccharomyces cerevisiae / growth & development
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Saccharomyces cerevisiae / physiology
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Sphingomyelins / biosynthesis
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Sphingomyelins / physiology
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Substrate Specificity
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Transformation, Genetic
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Transgenes
Substances
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Caenorhabditis elegans Proteins
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Ceramides
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Sphingomyelins
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Oxidoreductases
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HYL-2 ceramide synthase, C elegans
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dihydroceramide desaturase
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DAF-2 protein, C elegans
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Receptor, Insulin
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Oxygen