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阿维菌素与 RDL 在朱砂叶螨中的互作:靶标部位和抗性机制研究。

The interaction between abamectin and RDL in the carmine spider mite: a target site and resistant mechanism study.

机构信息

Academy of Agricultural Sciences, Southwest University, Chongqing 400716, China; College of Plant Protection, Southwest University, Chongqing 400716, China.

Department of Biology, Abilene Christian University, Abilene, TX 79699, USA.

出版信息

Pestic Biochem Physiol. 2020 Mar;164:191-195. doi: 10.1016/j.pestbp.2020.01.010. Epub 2020 Jan 23.

DOI:10.1016/j.pestbp.2020.01.010
PMID:32284126
Abstract

The γ-aminobutyric acid receptor (GABAR) has been identified as a target site of some commonly used insecticides. Our pervious study documented an interesting phenomenon, i.e. GABA accumulation was involved in abamectin resistance in the carmine spider mite, Tetranychus cinnabarinus. However, the mechanism of this phenomenon remains to be clarified. In this study, we investigated the interaction between abamectin and GABAR. Firstly, an artificial increase of GABA content was conducted in T. cinnabarinus and toxicity assays showed that GABA accumulation could indeed increase the tolerance of T. cinnabarinus to abamectin in vivo. Subsequently a GABAR of T. cinnabarinus, RDL2, was expressed in Xenopus oocytes and its sensitiveness to abamectin was detected. The results revealed that RDL2 showed significant responses to a series of GABA concentrations and GABA inhibited the effect of abamectin in vitro, providing direct evidence of the abamectin resistance mediated by GABA content. Our data confirmed that GABAR is the action target of abamectin and the GABA accumulation is one of the mechanisms of abamectin resistance in spider mites.

摘要

γ-氨基丁酸受体(GABAR)已被确定为一些常用杀虫剂的作用靶点。我们之前的研究记录了一个有趣的现象,即 GABA 积累参与了朱砂叶螨对阿维菌素的抗性。然而,这一现象的机制仍有待阐明。在这项研究中,我们研究了阿维菌素与 GABAR 的相互作用。首先,在朱砂叶螨中人为增加 GABA 含量,毒性测定表明,GABA 积累确实可以增加朱砂叶螨体内对阿维菌素的耐受性。随后,在非洲爪蟾卵母细胞中表达了朱砂叶螨的 GABAR,RDL2,并检测了其对阿维菌素的敏感性。结果表明,RDL2 对一系列 GABA 浓度表现出显著反应,GABA 抑制了阿维菌素在体外的作用,为 GABA 含量介导的阿维菌素抗性提供了直接证据。我们的数据证实 GABAR 是阿维菌素的作用靶标,GABA 积累是蜘蛛螨对阿维菌素产生抗性的机制之一。

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