CYP6CX3介导烟粉虱对溴氰虫酰胺的抗性机制及其表达调控机制

抗药性问题是烟粉虱及其传播的植物病毒病治理的难点。新一代双酰胺类杀虫剂溴氰虫酰胺已成为烟粉虱抗性治理的重要替代药剂，但田间抗性监测发现该害虫已对溴氰虫酰胺产生明显抗性。前期研究发现细胞色素P450基因CYP6CX3的过量表达与烟粉虱对溴氰虫酰胺的抗性密切相关。在此基础上，拟开展以下研究：1）利用RNAi和转基因果蝇技术，明确CYP6CX3过表达与烟粉虱对溴氰虫酰胺抗性的关系；2）构建CYP6CX3和P450还原酶共表达Sf9昆虫细胞系，解析其对溴氰虫酰胺的代谢活性，揭示CYP6CX3对溴氰虫酰胺的代谢机制；3）鉴定CYP6CX3基因的启动子序列和调控其转录的转录因子及miRNA，从转录水平和转录后水平揭示调控CYP6CX3基因表达的分子机制。研究成果将较为系统地揭示CYP6CX3在烟粉虱对溴氰虫酰胺抗性中的作用及其表达调控机制，有助于更为全面的了解烟粉虱对双酰胺类杀虫剂抗性的分子机制。

Insecticide resistance is a serious problem affecting the control of Bemisia tabaci and plant virus diseases spread by the pest. As a novel diamide insecticide, cyantraniliprole has become the first candidate for resistance management for B. tabaci, however, field populations of B. tabaci have developed high resistance to cyantraniliprole in recent years. Our preliminary study suggested that overexpression of CYP6CX3 was involved in the resistance to cyantraniliprole in B. tabaci. In this proposal, we want to 1) clarify the role of CYP6CX3 in resistance to cyantraniliprole by RNAi of CYP6CX3 in B. tabaci or overexpression in Drosophila melanogaster lines together with bioassay; 2) co-express the CYP6CX3 and CPR genes in Sf9 insect cells and determine the metabolic activity of expressed CYP6CX3 to cyantraniliprole to confirm its metabolic mechanism to cyantraniliprole; 3) identify the promotors, transcription factors and microRNAs that could regulate the expression of CYP6CX3. The expected results will reveal the roles of CYP6CX3 in cyantraniliprole resistance and the regulation mechanisms of its expression, which would provide helpful information for further understanding of the molecular mechanisms of diamide insecticides.