烟粉虱入侵我国十余年，其危害隐种已由早期入侵的B烟粉虱转化为后期入侵的Q烟粉虱，替代机制研究发现杀虫剂的使用是导致Q替代B的关键因子。本项目拟以B、Q敏感性存在显著差异的吡虫啉为代表性药剂，研究阐明杀虫剂驱动Q替代B的分子机理及其调控机制。即首先利用全基因组注释获得B、Q体内吡虫啉靶标nAChRs、代谢酶P450s、GST和CarE基因序列，并通过基因芯片检测、qRT-PCR验证并结合生物信息学分析，在基因组水平上筛选与吡虫啉抗性相关的关键遗传改变；并进一步克隆造成关键遗传改变的解毒酶或受体基因全长，构建其相应的表达载体，并通过转基因果蝇技术、代谢酶离体表达降解杀虫剂技术、RNAi、膜片钳和双荧光素酶报告基因分析系统，从基因组水平上阐明关键遗传改变的功能与其调控机理。研究结果对于阐明害虫对杀虫剂抗药性进化机制和烟粉虱等外来入侵生物的预防与控制具有重要的理论与实践意义。

The sweet potato whitefly, Bemisia tabaci (Gennadius) has been invaded in China more than ten years, in which cryptic species B and Q are the most invasive. In recent years, damages caused by cryptic species Q are more tremendous than the previous dominant cryptic species B. Previously study indicated that insecticides play a vital role in the competitive displacement of the two cryptic species. The proposed research is to clarify the molecular basis and regulation mechanisms of the insecticides-induced displacement (eg: Imidacloprid). First of all, DNA sequences of nicotinic acetylcholine receptors (nAChRs, the target site of imidacloprid), cytochrome P450 monooxygenases, Glutathione S-transferase (GST) and Carboxylesterase (CarE) are cloned from the database of whole genomic sequence project. Then, using the microarray, bioinformatics analysis and q-RT PCR to archive genes involved in the imidacloprid resistance, and clone their full-length sequences. In addition, methods molecular biology technologies of construction of transgenic fly strains, baculovirus-mediated gene expression, RNA interfere (RNAi), electrophysiological studies and dual-luciferase reporter gene system are carried out to clarify the molecular basis and regulation mechanisms of the two cryptic species displacement. The results of this study are of great theoretical and practical significance for the evolution of insecticide resistance mechanisms against whitefly and other exotic invasive species.