Molecular Mechanisms of Resistance to Diamide Insecticides in <i>Spodoptera litura</i>: Insights from Both Metabolic and Target-Site Resistance

Tiorantraniliprole is a novel diamide insecticide, and the resistance level and mechanism of <i>Spodoptera litura</i> to tiorantraniliprole and the multiresistance mechanism with other diamide insecticides are still unknown. In this study, bioassays showed that field <i>S. litura</i> developed high and medium levels of resistance to tiorantraniliprole, chlorantraniliprole, and cyantraniliprole. Enzyme activity and synergist bioassay indicated that P450s was the main factor leading to metabolic resistance to tiorantraniliprole. Transcriptome sequencing and qPCR showed that <i>CYP6B50</i> was upregulated by tiorantraniliprole induction and overexpressed in the field-resistant strain. RNA interference and transgenic fruit fly indicated that <i>CYP6B50</i> was involved in multiresistance to tiorantraniliprole, chlorantraniliprole, and cyantraniliprole. In addition, a target mutation site I4723M in RyR was detected in the field-resistant strain. Further genetic crossing and insecticides docking confirmed that the I4723M mutation involved in chlorantraniliprole and cyantraniliprole resistance also mediated resistance to tiorantraniliprole. This study comprehensively elucidated the mechanisms of resistance to diamide insecticides from both metabolic and target-site resistance in <i>S. litura</i>.