Bemisia tabaci is one of most notorious pests on various crops worldwide and many populations showed high resistance to different types of insecticides. Flupyradifurone is one novel insecticide against sucking pests. B. tabaci resistance to flupyradifurone has been detected in the field, however the mechanism of flupyradifurone resistance has rarely been studied.
The flupyradifurone-resistant strain (FLU-SEL) was selected from the susceptible strain of B. tabaci (MED-S) with 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. Our results of synergism tests and metabolic enzyme assays suggested that FLU-SEL resistance can be attributed to the enhanced detoxification mediated by glutathione S-transferase (GST) and P450 monooxygenase (P450). Compared with MED-S strain, CYP6CX4 and GSTs2 was significantly overexpressed in FLU-SEL, and silencing CYP6CX4 or GSTs2 increased the mortality of whiteflies to flupyradifurone challenge in FLU-SEL. Additionaly, silencing CYP6CX4 also increased the mortality of whiteflies to imidacloprid.
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. This article is protected by copyright. All rights reserved.

This article is protected by copyright. All rights reserved.

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