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Science 17 April 2009:
Vol. 324. no. 5925, pp. 381 - 384
DOI: 10.1126/science.1168532
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Reports

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

Vincent Menuz,1 Kate S. Howell,2,3 Sébastien Gentina,1 Sharon Epstein,2 Isabelle Riezman,2 Monique Fornallaz-Mulhauser,1 Michael O. Hengartner,4 Marie Gomez,5* Howard Riezman,2*{dagger} Jean-Claude Martinou1*{dagger}

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.

1 Department of Cell Biology, University of Geneva, CH-1211 Geneva 4, Switzerland.
2 Department of Biochemistry, University of Geneva, CH-1211 Geneva 4, Switzerland.
3 Faculty of Land and Food Resource, University of Melbourne, Parkville Victoria 3010, Australia.
4 Institute of Molecular Biology, University of Zurich, Winterthurerstrasse, CH-8057 Zurich, Switzerland.
5 Department of Zoology and Animal Biology, University of Geneva, CH-1211 Geneva 4, Switzerland.

* These authors contributed equally to this work.

{dagger} To whom correspondence should be addressed. E-mail: Howard.Riezman{at}unige.ch (H.R.); Jean-Claude.Martinou{at}unige.ch (J.-C.M.)

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Science. ISSN 0036-8075 (print), 1095-9203 (online)