Mutation V65I in the β1 Subunit of the Nicotinic Acetylcholine Receptor Confers Neonicotinoid and Sulfoxaflor Resistance in Insects

• DOI: 10.1021/acs.jafc.3c09456
• Publication Date: 2024-03-05T23:54:57Z
• Authors: Kun Zhang; Longwei Chen; Jianwen Chen; Huixiu Huang; Kaiyang Liu; Yi Zhang; Jingfang Yang; Shaoying Wu
• Keywords: Neonicotinoid

Neonicotinoids have been widely used to control pests with remarkable effectiveness. Excessive insecticides led serious insect resistance. Mutations of the nicotinic acetylcholine receptor (nAChR) are one reasons for neonicotinoid resistance conferred in various agricultural pests. Two mutations, V65I and V104I, were found nAChR β1 subunit two neonicotinoid-resistant aphid populations. However, specific functions mutations remain unclear. In this study, we cloned identified four subunits (α1, α2, α8, β1) thrips them be highly homologous other insects. Subsequently, successfully expressed subtypes (α1/α2/α8/β1 α1/α8/β1) by coinjecting three cofactors first time thrips, α1/α8/β1 showed abundant current rapidly. Acetylcholine, neonicotinoids, sulfoxaflor exhibited different activation capacities nAChRs. Finally, was significantly reduce binding ability neonicotinoids through electrophysiology computer simulations. V104I caused a decrease agonist affinity (pEC50) but an increase efficacy (Imax) against reduced sulfoxaflor. This study provides theoretical technical support studying molecular mechanisms