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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.
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Feng et al. (2019) studied this question.
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