Bt toxin resistance from loss of a putative carbohydrate-modifying enzyme
Bt toxin resistance from loss of a putative carbohydrate-modifying enzyme
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DOI：
10.1126/science.1062441
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发表时间：
2001-08-03
期刊：
影响因子：
56.9
通讯作者：
Aroian, RV
中科院分区：
文献类型：
--
作者：
Griffitts, JS;Whitacre, JL;Aroian, RV
抗性的发展是长期使用Bt毒素的主要威胁。在这里，我们报告的Bt毒素抗性基因，秀丽隐杆线虫bre-5，它编码一个假定的β-1，3-半乳糖基转移酶的克隆。肠道中缺乏bre-5导致对Bt毒素Cry 5 B的抗性。野生型而不是bre-5突变体动物被发现摄取毒素进入它们的肠道细胞，这与bre-5突变体在它们的顶肠上缺乏毒素结合位点相一致。bre-5突变体表现出对Cry 14 A的抗性，Cry 14 A是一种对线虫和昆虫都致命的Bt毒素;这表明通过碳水化合物修饰的丧失而产生的抗性与多种Bt毒素有关。
The development of resistance is the main threat to the long-term use of toxins from Bacillus thuringiensis (Bt) in transgenic plants. Here we report the cloning of a Bt toxin resistance gene, Caenorhabditis elegans bre-5, which encodes a putative beta -1,3-galactosyltransferase. Lack of bre-5 in the intestine led to resistance to the Bt toxin Cry5B. Wild-type but not bre-5 mutant animals were found to uptake toxin into their gut cells, consistent with bre-5 mutants lacking toxin-binding sites on their apical gut. bre-5 mutants displayed resistance to Cry14A, a Bt toxin lethal to both nematodes and insects; this indicates that resistance by loss of carbohydrate modification is relevant to multiple Bt toxins.