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First published online March 4, 2009

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Getting to grips with GSL function

Glycosphingolipids (GSLs) are thought to be essential membrane components in mammalian cells, and have been implicated in neuronal development, protein sorting and cell adhesion and migration on the basis of cell-culture experiments. However, it has been difficult to interpret data from mice that lack GSLs; for this reason, the role of GSLs in vivo is less clear. To address this issue, Giovanni Lesa and colleagues (p. 822) now create mutants of C. elegans in which all three genes encoding ceramide glucosyltransferases (CGTs; enzymes that catalyse a step in GSL biosynthesis) are either knocked out or knocked down. The authors show that worms lacking CGTs fail to produce GSLs and undergo growth arrest at the first larval stage. Moreover, a subset of cells in the digestive tract of mutant worms displays defects that impair larval feeding; this leads to a starvation-like phenotype. Notably, the authors show that the reintroduction of genes encoding CGTs to this subset – but not to other cells – rescues the growth-arrest phenotype, giving rise to worms that appear to be phenotypically normal. The authors conclude that, unexpectedly, GSLs are dispensable for most tissues in C. elegans, including the nervous system. Their results shed light on the role of GSLs in C. elegans and complement data from mammalian models of GSL deficiency.

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Related articles in JCS:

Expression of ceramide glucosyltransferases, which are essential for glycosphingolipid synthesis, is only required in a small subset of C. elegans cells

Esther Marza, Karina T. Simonsen, Nils J. Færgeman, and Giovanni M. Lesa
JCS 2009 122: 822-833. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?