Pest Management Science · 2019 · 46 citations · 48 references
Life SciencesEntomologyPharmacologyInsect EcologyInsect ToxicologyPesticide ToxicologyCytochrome P450 EnzymesCytochrome P450 InteractionsCytochrome P450-mediated MetabolismInsect ResistanceInsecticide ResistanceMolecular Basis Of ResistanceCytochrome P450 Enzyme InhibitionCytochrome P450 Expression RegulationCytochrome P450 InhibitionCytochrome P450 Reaction MechanismsCytochrome P450 Resistance
BACKGROUND: Acaricide resistance is a serious problem in spider mites. Cyflumetofen is a new complex II inhibitor, whereas pyridaben acts at complex I and has been used for decades. Although cross-resistance between cyflumetofen and pyridaben has been observed in Tetranychus cinnabarinus, the specific mechanisms at play have not yet been investigated. RESULTS: Investigation into the cross-resistance mechanisms identified five P450s, among which CYP389C16 was evaluated as the most likely candidate conferring cross-resistance. Knockdown of CYP389C16 expression via RNA interference diminished the level of cross-resistance in the cyflumetofen-resistant strain. In addition, recombinant CYP389C16 (40 pmol) effectively metabolized 25.0 ± 0.7% of cyflumetofen, 39.7 ± 1.0% of pyridaben, and 69.3 ± 3.3% of AB-1 (active de-esterified metabolite of cyflumetofen) within 2 h. In addition, hydroxylation metabolite of AB-1 was identified by HPLC-MS/MS. CONCLUSIONS: The study reveals that overexpressed CYP389C16 is involved in the cross-resistance between cyflumetofen and pyridaben in T. cinnabarinus. © 2019 Society of Chemical Industry.
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Life Sciences, Biology, Entomology +17