Their
discovery prompted the scientists to hypothesize that crystalline Bt
toxinswhich act by attacking and dissolving the intestines of their
hostnormally recognize the outer surface of intestinal cells by means
of carbohydrates or sugars. When the galactyosyltransferase gene is
missing, these sugars are not made and the toxin fails to recognize its host.
Resistant roundworms fed Bt toxin show no damage to internal structures, unlike the susceptible form.
Whether this enzyme is essential for many other Bt toxins remains to be determined. But the UCSD scientists discovered that their mutant roundworms were also resistant to a Bt toxin that is lethal to beetles, suggesting that the development of resistance by the loss of carbohydrate-modifying enzyme is relevant to insects as well. Furthermore the three dimensional structure of diverse insecticidal Bt toxins contains a fold that is predicted to bind precisely the sugar modification made by the galactosyltransferase, raising the possibility that this mechanism of resistance could be widespread. The discovery that the loss of a general modifier like a galactosyltransferase can allow an organism to develop resistance to Bt toxin is not good news.
"For
people using Bt toxins to control insects, this is a particularly threatening
scenario," says Aroian. "The reason is that with one swoop, you can knock
out the binding of multiple toxins to multiple receptors. But
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Contact: Kim McDonald
kimmcdonald@ucsd.edu
858-534-7572
University of California - San Diego
2-Aug-2001