Kwon D H, Yoon K S, Clark J M, Lee S H
Department of Agricultural Biotechnology, Seoul National University, Seoul, South Korea.
Insect Mol Biol. 2010 Aug;19(4):583-91. doi: 10.1111/j.1365-2583.2010.01017.x. Epub 2010 Jun 2.
The molecular mechanisms and genetics of abamectin resistance mediated by target site insensitivity in the two-spotted spider mite, Tetranychus urticae, were investigated by comparing two isogenic abamectin-susceptible (AbaS) and abamectin-resistant (AbaR) strains. Cloning and sequencing of full-length cDNA fragments of gamma-amino butyric acid (GABA)-gated chloride channel genes revealed no polymorphisms between the two strains. However, sequence comparison of the full-length cDNA fragment of a T. urticae glutamate-gated chloride channel gene (TuGluCl) identified a G323D point mutation as being tentatively related with abamectin resistance. In individual F(2) progenies obtained by backcrossing, the G323D genotype was confirmed to correlate with abamectin resistance. Bioassays using progeny from reciprocal crossings revealed that the abamectin resistance trait resulting from TuGluCl insensitivity is incompletely recessive.
通过比较两个等基因的阿维菌素敏感（AbaS）和阿维菌素抗性（AbaR）品系，研究了二斑叶螨对阿维菌素产生靶标位点不敏感介导的抗性分子机制和遗传学。γ-氨基丁酸（GABA）门控氯离子通道基因全长cDNA片段的克隆和测序显示，两个品系之间没有多态性。然而，二斑叶螨谷氨酸门控氯离子通道基因（TuGluCl）全长cDNA片段的序列比较确定了一个G323D点突变，初步认为与阿维菌素抗性有关。在回交获得的单个F(2)后代中，G323D基因型被证实与阿维菌素抗性相关。使用正反交后代进行的生物测定表明，由TuGluCl不敏感导致的阿维菌素抗性性状是不完全隐性的。
