Department of Evolutionary and Population Biology, Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, Amsterdam, The Netherlands.
Laboratory of Agrozoology, Department of Plants and Crops, Faculty of Bioscience Engineering, Ghent University, Ghent, Belgium.
Pest Manag Sci. 2020 Mar;76(3):1154-1163. doi: 10.1002/ps.5628. Epub 2019 Nov 13.
In spider mites, mutations in the mitochondrial cytochrome b Q pocket have been reported to confer resistance to the Q inhibitors bifenazate and acequinocyl. In this study, we surveyed populations of the two-spotted spider mite Tetranychus urticae for mutations in cytochrome b, linked newly discovered mutations with resistance and assessed potential pleiotropic fitness costs.
We identified two novel mutations in the Q site: G132A (equivalent to G143A in fungi resistant to strobilurins) and G126S + A133T (previously reported to cause bifenazate and acequinocyl resistance in Panonychus citri). Two T. urticae strains carrying G132A were highly resistant to bifenazate but not acequinocyl, whereas a strain with G126S + A133T displayed high levels of acequinocyl resistance, but only moderate levels of bifenazate resistance. Bifenazate and acequinocyl resistance were inherited maternally, providing strong evidence for the involvement of these mutations in the resistance phenotype. Near isogenic lines carrying G132A revealed several fitness penalties in T. urticae; a lower net reproductive rate (R ), intrinsic rate of increase (rm) and finite rate of increase (LM); a higher doubling time (DT); and a more male-biased sex ratio.
Several lines of evidence were provided to support the causal role of newly discovered cytochrome b mutations in bifenazate and acequinocyl resistance. Because of the fitness costs associated with the G132A mutation, resistant T. urticae populations might be less competitive in a bifenazate-free environment, offering opportunities for resistance management. © 2019 Society of Chemical Industry.
在叶螨中，已报道线粒体细胞色素 b Q 口袋中的突变赋予了对 Q 抑制剂双甲脒和螺虫乙酯的抗性。在这项研究中，我们调查了二斑叶螨 Tetranychus urticae 种群中细胞色素 b 的突变情况，将新发现的突变与抗性联系起来，并评估了潜在的多效性适应代价。
我们在 Q 位点鉴定出两个新的突变：G132A（相当于对杀真菌剂 strobilurins 具有抗性的真菌中的 G143A）和 G126S+A133T（先前报道在柑橘全爪螨 Panonychus citri 中导致双甲脒和螺虫乙酯抗性）。两个携带 G132A 的 T. urticae 菌株对双甲脒高度抗性但对螺虫乙酯无抗性，而携带 G126S+A133T 的菌株对螺虫乙酯表现出高水平的抗性，但对双甲脒的抗性仅为中等水平。双甲脒和螺虫乙酯抗性是母系遗传的，这为这些突变参与抗性表型提供了有力证据。携带 G132A 的近等基因系在 T. urticae 中显示出几个适应代价；净生殖率（R）、内禀增长率（rm）和有限增长率（LM）较低；倍增时间（DT）较高；以及更偏向雄性的性别比例。
提供了几条证据来支持新发现的细胞色素 b 突变在双甲脒和螺虫乙酯抗性中的因果作用。由于与 G132A 突变相关的适应代价，具有抗性的 T. urticae 种群在没有双甲脒的环境中可能竞争力较弱，为抗性管理提供了机会。 © 2019 化学工业协会。
