Background: Bemisia tabaci is 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. tabaci resistance 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 of B. 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 glutathione S-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. © 2020 Society of Chemical Industry.
Keywords: Bemisia tabaci; RNA interference; cytochrome P450s monooxygenase; flupyradifurone; glutathione S-transferase; metabolic resistance.
© 2020 Society of Chemical Industry.