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首页> 外文期刊>Bulletin of Entomological Research >Characterization of the M918T sodium channel gene mutation associated with strong resistance to pyrethroid insecticides in the peach-potato aphid, Myzus persicae (Sulzer).
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Characterization of the M918T sodium channel gene mutation associated with strong resistance to pyrethroid insecticides in the peach-potato aphid, Myzus persicae (Sulzer).

机译:M918T钠通道基因突变的特征与桃蚜,桃蚜(Sulzer)中对拟除虫菊酯类杀虫剂的强抗性相关。

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摘要

Recent advances in the characterisation of insect sodium channel gene sequences have identified a small number of point mutations within the channel protein that are implicated in conferring target-site resistance to pyrethroid insecticides (so-called knockdown resistance or kdr). The L1014F (leucine-to-phenylalanine) mutation located in the centre of segment 6 of the domain II region (IIS6) of the sodium channel (the so-called kdr trait) has been detected in the peach-potato aphid, Myzus persicae (Sulzer), and is considered to be the primary cause of pyrethroid resistance in this species. Here we report on the characterisation of a second mutation, M918T (methione-to-threonine), within the nearby IIS4-S5 intracellular linker (the so-called super-kdr trait) in a field clone also possessing L1014F, with both mutations present in heterozygous form. The resistance phenotype of M. persicae clones possessing various combinations of L1014F and M918T to a wide range of pyrethroids (both Type I and II) was assessed in leaf-dip bioassays and to lambda-cyhalothrin applied at up to ten times the recommended field rate as foliar sprays to aphids feeding on whole plants. Bioassay results demonstrated that presence of both mutations was associated with extreme resistance to all the pyrethroids tested relative to aphids lacking the mutations. Furthermore, this resistance well exceeded that shown by aphids that were homozygous for L1014F but lacking M918T. However, pre-treatment with piperonyl butoxide in the leaf-dip bioassays failed to suppress pyrethroid resistance in aphids carrying one or both of the mutations. The relevance of these findings for monitoring and managing pyrethroid resistance in M. persicae populations in the field is discussed.
机译:昆虫钠通道基因序列表征的最新进展已经确定了通道蛋白内的少量点突变,这些突变与赋予拟除虫菊酯类杀虫剂目标位点抗性(所谓的敲低抗性或kdr)有关。 L1014F(亮氨酸到苯丙氨酸)突变位于桃通道的桃蚜(Myzus persicae()中,位于钠通道II区(IIS6)区域II区(IIS6)的片段6的中心。 (Sulzer),并且被认为是该物种中拟除虫菊酯抗药性的主要原因。在这里,我们报告了在同样具有L1014F的野外克隆中,在附近的IIS4-S5细胞内连接子(所谓的super-kdr性状)内第二个突变M918T(甲硫氨酸到苏氨酸)的特征。以杂合形式存在。在叶浸式生物测定法中评估了具有L1014F和M918T的各种组合的百日咳博德特氏菌克隆对广泛的拟除虫菊酯(I型和II型)的抗性表型,对λ-氟氯氰菊酯的抗性表型是推荐田间速率的十倍作为叶面喷雾剂,以蚜虫为食以整株植物为食。生物测定结果表明,相对于缺乏突变的蚜虫,两种突变的存在均与对所有拟除虫菊酯的极端抗性相关。此外,这种抗性远远超过了对L1014F纯合但缺乏M918T的蚜虫所显示的抗性。然而,在叶浸式生物测定中用胡椒基丁醚进行的预处理未能抑制携带一种或两种突变的蚜虫的拟除虫菊酯抗性。讨论了这些发现与监测和管理田间桃蚜种群中拟除虫菊酯抗性的相关性。

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