Mutation V65I in the β1 Subunit of the Nicotinic Acetylcholine Receptor Confers Neonicotinoid and Sulfoxaflor Resistance in Insects
文献类型： 外文期刊
作者： Zhang, Kun 1 ; Chen, Longwei 1 ; Chen, Jianwen 1 ; Huang, Huixiu 1 ; Liu, Kaiyang 1 ; Zhang, Yi 1 ; Yang, Jingfang 3 ; Wu, Shaoying 1 ;
作者机构： 1.Hainan Univ, Sanya Inst Breeding & Multiplicat, Sch Breeding & Multiplicat, Sanya 572024, Peoples R China
2.Hainan Univ, Sch Trop Agr & Forestry, Sch Agr & Rural Affairs, Sch Rural Revitalizat, Danzhou 571700, Peoples R China
3.Chinese Acad Agr Sci, Inst Plant Protect, State Key Lab Biol Plant Dis & Insect Pests, Beijing 100193, Peoples R China
4.Chinese Acad Agr Sci, Natl Nanfan Res Inst, Sanya 572024, Peoples R China
关键词： Megalurothrips usitatus; nicotinicacetylcholine receptor; insecticide resistance; electrophysiology; computer modeling
期刊名称：JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY （ 影响因子：6.1； 五年影响因子：6.3 ）
ISSN： 0021-8561
年卷期： 2024 年 72 卷 11 期
页码：
收录情况： SCI
摘要： Neonicotinoids have been widely used to control pests with remarkable effectiveness. Excessive insecticides have led to serious insect resistance. Mutations of the nicotinic acetylcholine receptor (nAChR) are one of the reasons for neonicotinoid resistance conferred in various agricultural pests. Two mutations, V65I and V104I, were found in the nAChR beta 1 subunit of two neonicotinoid-resistant aphid populations. However, the specific functions of the two mutations remain unclear. In this study, we cloned and identified four nAChR subunits (alpha 1, alpha 2, alpha 8, and beta 1) of thrips and found them to be highly homologous to the nAChR subunits of other insects. Subsequently, we successfully expressed two subtypes nAChR (alpha 1/alpha 2/alpha 8/beta 1 and alpha 1/alpha 8/beta 1) by coinjecting three cofactors for the first time in thrips, and alpha 1/alpha 8/beta 1 showed abundant current rapidly. Acetylcholine, neonicotinoids, and sulfoxaflor exhibited different activation capacities for the two subtypes of nAChRs. Finally, V65I was found to significantly reduce the binding ability of nAChR to neonicotinoids and sulfoxaflor through electrophysiology and computer simulations. V104I caused a decrease in agonist affinity (pEC(50)) but an increase in the efficacy (I-max) of nAChR against neonicotinoids and reduced the binding ability of nAChR to sulfoxaflor. This study provides theoretical and technical support for studying the molecular mechanisms of neonicotinoid resistance in pests.
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