我国棉蚜对吡虫啉和氟啶虫胺腈抗性水平监测与交互抗性分析

为了解我国不同地区棉蚜Aphis gossypii对吡虫啉和氟啶虫胺腈的抗性现状，对代表性棉区棉蚜田间种群进行抗药性监测，同时通过构建具有R81T及V62I单突变和R81T-V62I共同突变的棉蚜烟碱型乙酰胆碱受体（nicotinic acetylcholine receptor，nAChR）蛋白模型，与吡虫啉和氟啶虫胺腈进行分子对接，分析这些突变在吡虫啉和氟啶虫胺腈抗性中的作用，并分析吡虫啉和氟啶虫胺腈之间是否存在交互抗性。结果显示，不同地区棉蚜对吡虫啉产生了高水平抗性，抗性倍数为174.70~56 409.18，对氟啶虫胺腈产生了低至中等水平抗性，抗性倍数为7.35~44.63，说明不同地区的棉蚜对氟啶虫胺腈的敏感度高于吡虫啉，且吡虫啉抗性和氟啶虫胺腈抗性间不存在相关性。R81T、V62I单突变和R81T-V62I共同突变导致吡虫啉与棉蚜nAChR的亲和力降低，对氟啶虫胺腈与棉蚜nAChR的结合无明显影响。R81T及V62I单突变和R81T-V62I共同突变导致棉蚜对吡虫啉产生靶标抗性，但是对氟啶虫胺腈的抗性无明显影响，这些突变不会导致吡虫啉与氟啶虫胺腈产生靶标突变的交互抗性。

Determination of resistance and cross-resistance to imidacloprid and sulfoxaflor in field populations of Aphis gossypii in China

To monitor the resistance levels of Aphis gossypii to insecticides imidacloprid and sulfoxaflor, various field populations in typical cotton planting areas of China were assessed, and the nicotinic acetylcholine receptor (nAChR) protein models of A. gossypii which contain R81T mutation alone, V62I mutation alone and R81T-V62I combined mutation were built and used to dock with imidacloprid and sulfoxaflor molecules. The effects of R81T mutation alone, V62I mutation alone and R81T-V62I combined mutations of nAChR were analyzed for the resistance to imidacloprid and to sulfoxaflor, and for the cross-resistance between imidacloprid and sulfoxaflor. The results showed that the different field populations of A. gossypii had developed high levels of resistance to imidacloprid, the resistance ratios ranged from 174.70 to 56 409.18. And low to moderate levels of resistance to sulfoxaflor were observed, the resistance ratios were 7.35-44.63. The resistance monitoring results indicated that the sensitivity of A. gossypii to sulfoxaflor was higher than that to imidacloprid in different field populations. Regression analysis showed that there was no significant correlation between the resistance to imidacloprid and the resistance to sulfoxaflor. The R81T mutation alone, V62I mutation alone and R81T-V62I combined mutations reduced the affinity of imidacloprid with nAChR, but had no significant effects on the sulfoxaflor binding with nAChR. The results suggested that the R81T mutation alone, V62I mutation alone and R81T-V62I combined mutations caused target-resistance to imidacloprid, but had no obvious effects on the resistance to sulfoxaflor. R81T, V62I and R81T-V62I mutations did not produced cross-resistance between imidacloprid and sulfoxaflor.