Journal
SCIENCE
Volume 324, Issue 5925, Pages 381-384Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1168532
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Funding
- Swiss National Science Foundation [3100A0-109419/2, 3100A0-114189, 3100A0-105907/1, 3100A0-113889]
- Human Frontiers Science Program Organization
- Swiss SystemsX.ch initiative
- Roche Foundation
- Ernest Boninchi
- Canton of Zurich
- Ernst Hadorm Foundation
- Geneva Department of Education
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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.
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