1. Resistance is non-futile: resistance to Cry5B in the nematode Caenorhabditis elegans.
- Author
-
Barrows BD, Griffitts JS, and Aroian RV
- Subjects
- Animals, Bacillus thuringiensis Toxins, Bacterial Proteins metabolism, Bacterial Toxins metabolism, Caenorhabditis elegans Proteins metabolism, Clone Cells, Cloning, Molecular, Endotoxins metabolism, Glycolipids genetics, Glycolipids metabolism, Glycosylation, Glycosyltransferases metabolism, Hemolysin Proteins metabolism, Mutation, Bacterial Proteins genetics, Bacterial Toxins genetics, Caenorhabditis elegans microbiology, Caenorhabditis elegans Proteins genetics, Endotoxins genetics, Glycosyltransferases genetics, Hemolysin Proteins genetics, Insecticide Resistance genetics, Pest Control, Biological
- Abstract
The nematode, Caenorhabditis elegans, can be mutated to resistance to the Cry5B toxin of Bacillus thuringiensis. By cloning and characterization of these C. elegans resistance genes, we have determined that a major mechanism by which C. elegans resists Cry5B is by loss of function mutations in any one of four gylcosyltransferase genes that glycosylate glycolipids specific to arthropods. Without correct gylcosylation, binding of Cry5B is greatly impaired in C. elegans. That these specific arthroseries glycolipids do not occur in vertebrates potentially helps explain why Cry toxins are specific for arthropods.
- Published
- 2007
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