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线粒体编码细胞色素 b 中的 G126S 取代不会赋予叶螨 Tetranychus urticae 对双甲脒的抗性。

The G126S substitution in mitochondrially encoded cytochrome b does not confer bifenazate resistance in the spider mite Tetranychus urticae.

机构信息

Department of Plants and Crops, Faculty of Bioscience Engineering, Ghent University, Coupure Links 653, 9000, Ghent, Belgium.

Terrestrial Ecology Unit, Department of Biology, Faculty of Science, Ghent University, K.L. Ledeganckstraat 35, 9000, Ghent, Belgium.

出版信息

Exp Appl Acarol. 2021 Dec;85(2-4):161-172. doi: 10.1007/s10493-021-00668-6. Epub 2021 Oct 25.

DOI:10.1007/s10493-021-00668-6
PMID:34693496
Abstract

Several genetic variants of the cd1- and ef-helices of the Q site of mitochondrial cytochrome b have been associated with bifenazate resistance in the spider mite Tetranychus urticae, an important crop pest around the world. Maternal inheritance of bifenazate resistance has provided strong evidence for the involvement of many of these mutations alone or in combination. A number of populations highly resistant to bifenazate were uncovered that carried the G126S substitution in combination with other target-site mutations. This G126S mutation has therefore been investigated in several studies in the context of resistance evolution and the development of diagnostic markers. However, experimental data that link bifenazate resistance with the presence of the G126S mutation without additional cd1- and ef-helices mutations, remain very limited. Here, we genotyped 38 T. urticae field populations for cytochrome b and uncovered nine field populations with a fixed or segregating G126S substitution without other target-site mutations in the conserved cd1- and ef-helices of the cytochrome b Q pocket. Toxicity bioassays showed that all nine field populations were very susceptible to bifenazate, providing strong evidence that G126S alone does not confer bifenazate resistance. These findings also implicate that previous T. urticae populations with G126S found to be low to moderately resistant to bifenazate, evolved alternative mechanisms of resistance, and more importantly, that this mutation cannot be used as a molecular diagnostic for bifenazate resistance.

摘要

线粒体细胞色素 b 的 Q 位点的 cd1-和 ef-螺旋中的几个遗传变异与蜘蛛螨 Tetranychus urticae 对双甲脒的抗性有关,这种螨是全球重要的作物害虫。双甲脒抗性的母系遗传为这些突变单独或组合参与提供了强有力的证据。许多对双甲脒高度抗性的种群被发现,这些种群携带 G126S 取代与其他靶标突变相结合。因此,在一些研究中,G126S 突变在抗性进化和诊断标记的开发背景下进行了研究。然而,将双甲脒抗性与 G126S 突变的存在联系起来的实验数据,而没有额外的 cd1-和 ef-螺旋突变,仍然非常有限。在这里,我们对 38 个 T. urticae 田间种群进行了细胞色素 b 基因分型,发现了 9 个田间种群存在固定或分离的 G126S 取代,而细胞色素 b Q 袋中的保守 cd1-和 ef-螺旋中没有其他靶标突变。毒性生物测定表明,所有 9 个田间种群对双甲脒非常敏感,这为 G126S 单独不赋予双甲脒抗性提供了强有力的证据。这些发现还表明,以前发现对双甲脒具有低至中度抗性的具有 G126S 的 T. urticae 种群,已经进化出了替代的抗性机制,更重要的是,该突变不能用作双甲脒抗性的分子诊断。

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