Barrows Brad D, Griffitts Joel S, Aroian Raffi V
Section of Cell and Developmental Biology, University of California, San Diego, La Jolla, CA 92093-0349, USA.
J Invertebr Pathol. 2007 Jul;95(3):198-200. doi: 10.1016/j.jip.2007.04.002. Epub 2007 Apr 6.
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.
线虫秀丽隐杆线虫(Caenorhabditis elegans)可通过突变获得对苏云金芽孢杆菌(Bacillus thuringiensis)Cry5B毒素的抗性。通过克隆和鉴定这些秀丽隐杆线虫抗性基因,我们已确定,秀丽隐杆线虫抵抗Cry5B的主要机制是四个糖基转移酶基因中任何一个发生功能丧失突变,这些基因可对节肢动物特有的糖脂进行糖基化修饰。没有正确的糖基化修饰,Cry5B在秀丽隐杆线虫中的结合会受到极大损害。这些特定的节肢动物系列糖脂在脊椎动物中不存在,这可能有助于解释为什么Cry毒素对节肢动物具有特异性。