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Characterization of flupyradifurone resistance in the whitefly Bemisia tabaci Mediterranean (Q biotype)
Author(s) -
Wang Ran,
Wang Jinda,
Zhang Jiasong,
Che Wunan,
Feng Honglin,
Luo Chen
Publication year - 2020
Publication title -
pest management science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.296
H-Index - 125
eISSN - 1526-4998
pISSN - 1526-498X
DOI - 10.1002/ps.5995
Subject(s) - imidacloprid , biology , cross resistance , microbiology and biotechnology , virology , pesticide , agronomy
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