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Protection of C. elegans from Anoxia by HYL-2 Ceramide Synthase

2009; American Association for the Advancement of Science; Volume: 324; Issue: 5925 Linguagem: Inglês

10.1126/science.1168532

1095-9203

Vincent Menuz, Kate Howell, Sébastien Gentina, Sharon Epstein, Isabelle Riezman, Monique Fornallaz-Mulhauser, Michael O. Hengartner, Marie Gomez, Howard Riezman, Jean‐Claude Martinou,

Sleep and Wakefulness Research

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.