The oriental fruit fly, Bactrocera dorsalis (Hendel), is a highly invasive and destructive pest. Chlorfenapyr is a widely used insecticide that disrupts mitochondrial activity. The Parkin protein plays conserved roles in maintaining mitochondrial homeostasis, but the role of Parkin in response to chlorfenapyr remains largely unknown. Here, we report that BdParkin is required for chlorfenapyr detoxification, and dsRNA targeting BdParkin improves the insecticidal efficacy of chlorfenapyr. Among the genes whose expression levels are affected by BdParkin RNAi, knock-down of the glutathione S-transferase gene BdGSTd2 increases the insecticidal efficacy of chlorfenapyr. Molecular docking reveals potential interactions between BdGSTd2 and tralopyril, an insecticidal metabolite of chlorfenapyr. These results suggest that BdParkin could impact the response of B. dorsalis to chlorfenapyr through metabolic processes regulated by BdGSTd2. Our findings could offer new insights into how insects detoxify chlorfenapyr and provide molecular targets for developing a sustainable management strategy for B. dorsalis.
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