Symbiotic bacteria are important drivers of phenotypic diversity in insects. One of the widespread symbionts to have emerged belongs to the genus Arsenophonus, however, its biological functions in most host insects remain entirely unknown. Here we report two distinct Arsenophonus strains in the brown planthopper (BPH), Nilaparvata lugens, a major pest insect in Asian countries that causes significant economic damage through rice crop destruction. Genomic resequencing data suggested that one Arsenophonus strain (S-type) negatively affected the insecticide resistance of the host. Indeed, replacement of the resident Arsenophonus with the S-type Arsenophonus significantly decreased host insecticide resistance. Transcriptome and metabolome analysis revealed down-regulation of xenobiotic metabolism and increased amino acid accumulation in the S-type Arsenophonus infected host. This study demonstrates how a symbiont-mediated phenotypic change can occur. The results of this study will aid in developing strategies that work through imposing an ecological disadvantage on insect pests, which will be of great value for pest control in agricultural industry.

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The cytochrome P450 CYP6ER1 has been reported to play an important role in imidacloprid resistance of the brown planthopper (BPH), Nilaparvata lugens , and is overexpressed in most resistant populations. In the present study, we confirmed that CYP6ER1 expression can be induced by certain levels of imidacloprid. Developmental expression analysis revealed that CYP6ER1 was expressed highly in the adult stage, and tissue distribution analysis showed that CYP6ER1 was expressed mainly in the fat body and midgut. RNA interference (RNAi) of CYP6ER1 and transgenic expression of CYP6ER1 in Drosophila melanogaster both suggested that the expression of CYP6ER1 is sufficient to confer imidacloprid resistance. Furthermore, we analyzed the interaction of imidacloprid and CYP6ER1 monooxygenase by using dynamic simulations and molecular docking. We found that Nitrogen atoms in the heterocycle of the imidacloprid molecule may bind to iron atoms in the center of the homology model of CYP6ER1 via 4,5-dihedro-1H-imidazole. This finding contributes to a better understanding of how CYP6ER1 takes part in the insecticide metabolism.

Imidacloprid resistance in the brown planthopper, Nilaparvata lugens, is primarily the result of the over-expression of cytochrome P450 monooxygenases. Here, a field-collected strain of N. lugens was shown to be highly resistant to both imidacloprid and buprofezin. Insecticide exposure and quantitative real-time PCR revealed that its resistance was mainly associated with a cytochrome P450 gene, CYP6AY1. CYP6AY1 is known to metabolize imidacloprid but its effect on buprofezin is unclear. In the 5'-untranslated region of CYP6AY1, a novel alternative splicing was detected. After a 1990-bp promoter region was cloned, its basal luciferase activity was assessed. Furthermore, genotyping studies identified 12 variations in the promoter region that discriminated between the field-collected and control strain. Finally, survival bioassays revealed a single nucleotide polymorphism and an insertion-deletion polymorphism linked to buprofezin and imidacloprid resistance. Mutagenesis of these sites enhanced the promoter activity of CYP6AY1. These results suggest that promoter polymorphisms may affect P450-mediated multiple insecticide resistance of pests.