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J. Biol. Chem., Vol. 282, Issue 5, 3302-3311, February 2, 2007

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Resistance to Bacillus thuringiensis Toxin in Caenorhabditis elegans from Loss of Fucose^*

Brad D. Barrows, Stuart M. Haslam, Larry J. Bischof, Howard R. Morris^¶, Anne Dell¹, and Raffi V. Aroian²

From the Section of Cell and Developmental Biology, University of California, San Diego, La Jolla, California 92093-0349, Division of Molecular Biosciences, Faculty of Natural Sciences, Imperial College London, London SW7 2AZ, United Kingdom, and ^¶M-SCAN Research and Training Center, Silwood Park, Ascot SL5 7PZ, United Kingdom

A mutation in the Caenorhabditis elegans bre-1 gene was isolated in a screen for Bacillus thuringiensis toxin-resistant (bre) mutants to the Cry5B crystal toxin made by B. thuringiensis. bre-1 mutant animals are different from the four other cloned bre mutants in that their level of resistance is noticeably lower. bre-1 animals also display a significantly reduced brood size at 25 °C. Here we cloned the bre-1 gene and characterized the bre-1 mutant phenotype. bre-1 encodes a protein with significant homology to a GDP-mannose 4,6-dehydratase, which catalyzes the first step in the biosynthesis of GDP-fucose from GDP-mannose. Injection of GDP-fucose but not fucose into C. elegans intestinal cells rescues bre-1 mutant phenotypes. Thus, C. elegans lacks a functional fucose salvage pathway. Furthermore, we demonstrate that bre-1 mutant animals are defective in production of fucosylated glycolipids and that bre-1 mutant animals make quantitatively reduced levels of glycolipid receptors for Cry5B. We finally show that bre-1 mutant animals, although viable, show a lack of fucosylated N- and O-glycans, based on mass spectrometric evidence. Thus, C. elegans can survive with little fucose and can develop resistance to crystal toxin by loss of a monosaccharide biosynthetic pathway.

Received for publication, July 12, 2006 , and in revised form, November 9, 2006.

^* This work was supported by National Science Foundation Grant MCB-0517718 (to R. V. A.), the Biotechnology and Biological Sciences Research Council, and Wellcome Trust grants (to A. D., H. R. M., and S. M. H.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Biotechnology and Biological Sciences Research Council Professorial Fellow.

² To whom correspondence should be addressed: Section of Cell and Developmental Biology, 9500 Gilman Dr., Dept. 0349, Bonner Hall 4430, La Jolla, CA 92093-0349. Tel.: 858-822-1396; Fax: 858-822-3021; E-mail: raroian{at}ucsd.edu.

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