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First published online 24 February 2009
doi: 10.1242/jcs.042754
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Research Article |
1 MRC Laboratory for Molecular Cell Biology, University College London, Gower Street, London WC1E 6BT, UK
3 Department of Cell and Developmental Biology, University College London, Gower Street, London WC1E 6BT, UK
2 University of Southern Denmark, Department of Biochemistry and Molecular Biology, Campusvej 55, 5230 Odense, Denmark
* Author for correspondence (e-mail: Giovanni.Lesa{at}ucl.ac.uk)
Accepted 26 November 2008
Glycosphingolipids (GSLs) are glycosylated derivatives of ceramide in the lipid bilayer. Their ubiquitous distribution and complexity suggest that they have important functions, but what these are in vivo is still poorly understood. Here, we characterize the phenotype of Caenorhabditis elegans mutants with essentially no GSLs. The C. elegans genome encodes three ceramide glucosyltransferase (CGT) genes, which encode enzymes required for GSL biosynthesis. Animals lacking CGT do not synthesize GSLs, arrest growth at the first larval stage, and display defects in a subset of cells in their digestive tract; these defects impair larval feeding, resulting in a starvation-induced growth arrest. Restoring CGT function in these digestive tract cells – but not in a variety of other tissues – is sufficient to rescue the phenotypes associated with loss of CGT function. These unexpected findings suggest that GSLs are dispensable in most C. elegans cells, including those of the nervous system.
Key words: C. elegans, Ceramide, Glycosphingolipids, Glycosyltransferase, Intestine
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