Characterization of flupyradifurone resistance in the whiteflyBemisia tabaciMediterranean (Q biotype)
文献类型： 外文期刊
作者： Wang, Ran 1 ; Wang, Jinda 2 ; Zhang, Jiasong 2 ; Che, Wunan 3 ; Feng, Honglin 4 ; Luo, Chen 1 ;
作者机构： 1.Beijing Acad Agr & Forestry Sci, Inst Plant & Environm Protect, Beijing 100097, Peoples R China
2.Fujian Agr & Forestry Univ, Natl Engn Res Ctr Sugarcane, Fuzhou, Peoples R China
3.Shenyang Agr Univ, Dept Pesticide Sci, Shenyang, Peoples R China
4.Boyce Thompson Inst Plant Res, Ithaca, NY USA
关键词： Bemisia tabaci; flupyradifurone; metabolic resistance; cytochrome P450s monooxygenase; glutathioneS-transferase; RNA interference
期刊名称：PEST MANAGEMENT SCIENCE （ 影响因子：4.845； 五年影响因子：4.674 ）
ISSN： 1526-498X
年卷期： 2020 年 76 卷 12 期
页码：
收录情况： SCI
摘要： BACKGROUND Bemisia tabaciis one of most notorious pests on various crops worldwide and many populations show high resistance to different types of insecticides. Flupyradifurone is a novel insecticide against sucking pests.B. tabaciresistance to flupyradifurone has been detected in the field, however the mechanism of flupyradifurone resistance has rarely been studied. RESULTS The flupyradifurone-resistant strain (FLU-SEL) was selected from the susceptible strain ofB. tabaci(MED-S) using flupyradifurone for 24 generations. The FLU-SEL strain exhibited 105.56-fold resistance to flupyradifurone, and moderate cross-resistance to imidacloprid, but no cross-resistance to other tested neonicotinoids. Synergism tests and metabolic enzyme assays suggested that FLU-SEL resistance can be attributed to enhanced detoxification mediated by glutathioneS-transferase (GST) and P450 monooxygenase (P450). Compared with MED-S strain, CYP6CX4 and GSTs2 were significantly overexpressed in FLU-SEL, and silencing CYP6CX4 or GSTs2 increased the mortality of whiteflies to flupyradifurone challenge in FLU-SEL. In addition, silencing CYP6CX4 also increased the mortality of whiteflies exposed to imidacloprid. CONCLUSION Overexpression of CYP6CX4 and GSTs2 was associated with flupyradifurone resistance, as confirmed by RNA interference. Our findings suggested that metabolic resistance to flupyradifurone might be mediated by P450s and GSTs.
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