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核受体NR2E的激活剂HR83可导致褐飞虱通过代谢解毒作用产生对毒死蜱的抗性。

Activation of the NR2E nuclear receptor HR83 leads to metabolic detoxification-mediated chlorpyrifos resistance in Nilaparvata lugens.

作者信息

Lu Kai, Li Yimin, Cheng Yibei, Li Wenru, Song Yuanyuan, Zeng Rensen, Sun Zhongxiang

机构信息

State Key Laboratory of Ecological Pest Control for Fujian and Taiwan Crops, College of Life Sciences, Fujian Agriculture and Forestry University, Fuzhou 350002, China.

Key Laboratory of Ministry of Education for Genetics, Breeding and Multiple Utilization of Crops, College of Agriculture, Fujian Agriculture and Forestry University, Fuzhou 350002, China.

出版信息

Pestic Biochem Physiol. 2021 Mar;173:104800. doi: 10.1016/j.pestbp.2021.104800. Epub 2021 Feb 8.

DOI:10.1016/j.pestbp.2021.104800
PMID:33771269
Abstract

Increased production of detoxification enzymes appears to be the primary route for insecticide resistance in many crop pests. However, the mechanisms employed by resistant insects for overexpression of detoxification genes involved in insecticide resistance remain obscure. We report here that the NR2E nuclear receptor HR83 plays a critical role in chlorpyrifos resistance by regulating the expression of detoxification genes in the brown planthopper (BPH), Nilaparvata lugens. HR83 was highly expressed in the fat body and ovary of adult females in chlorpyrifos-resistant BPHs. Knockdown of HR83 by RNA interference showed no effect on female fecundity, whereas caused a decrease of resistance to chlorpyrifos. This treatment also led to a dramatic reduction in the expression of multiple detoxification genes, including four UDP-glycosyltransferases (UGTs), three cytochrome P450 monooxygenases (P450s) and four carboxylesterases (CarEs). Among these HR83-regulated genes, UGT-1-3, UGT-2B10, CYP6CW1, CYP4CE1, CarE and Esterase E4-1 were over-expressed both in the fat body and ovary of the resistant BPHs. Functional analyses revealed that UGT-2B10, CYP4CE1, CarE and Esterase E4-1 are essential for the resistance of BPH to chlorpyrifos. Generally, this study implicates HR83 in the metabolic detoxification-mediated chlorpyrifos resistance and suggests that the regulation of detoxification genes may be an ancestral function of the NR2E nuclear receptor subfamily.

摘要

在许多农作物害虫中,解毒酶产量的增加似乎是抗杀虫剂的主要途径。然而,抗性昆虫用于过表达参与抗杀虫剂的解毒基因的机制仍不清楚。我们在此报告,NR2E核受体HR83通过调节褐飞虱(BPH)Nilaparvata lugens中解毒基因的表达,在对毒死蜱的抗性中起关键作用。HR83在抗毒死蜱的褐飞虱成年雌性的脂肪体和卵巢中高表达。通过RNA干扰敲低HR83对雌性繁殖力没有影响,但导致对毒死蜱的抗性降低。这种处理还导致多个解毒基因的表达显著降低,包括四种UDP-糖基转移酶(UGT)、三种细胞色素P450单加氧酶(P450)和四种羧酸酯酶(CarE)。在这些受HR83调控的基因中,UGT-1-3、UGT-2B10、CYP6CW1、CYP4CE1、CarE和酯酶E4-1在抗性褐飞虱的脂肪体和卵巢中均过表达。功能分析表明,UGT-2B10、CYP4CE1、CarE和酯酶E4-1对褐飞虱对毒死蜱的抗性至关重要。总体而言,本研究表明HR83参与代谢解毒介导的毒死蜱抗性,并表明解毒基因的调控可能是NR2E核受体亚家族的原始功能。

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Activation of the NR2E nuclear receptor HR83 leads to metabolic detoxification-mediated chlorpyrifos resistance in Nilaparvata lugens.核受体NR2E的激活剂HR83可导致褐飞虱通过代谢解毒作用产生对毒死蜱的抗性。
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