Abstract

Pymetrozine is commonly used for the control of Nilaparvata lugens, and resistance to pymetrozine has been frequently reported in the field populations in recent years. However, the mechanism of brown planthopper resistance to pymetrozine is still unknown. In this study, a pymetrozine-resistant strain (PMR) was established, and the potential biochemical resistance mechanism of N. lugens to pymetrozine was investigated. Pymetrozine was synergized by the inhibitor piperonyl butoxide (PBO) in the PMR with 2.83-fold relative synergistic ratios compared with the susceptible strain (Sus). Compared with the Sus, the cytochrome P450 monooxygenase activity of PMR was increased by 1.7 times, and two P450 genes (NlCYP6CS1 and NlCYP301B1) were found to be significantly overexpressed more than 6.0-fold in the PMR. Pymetrozine exposure induced upregulation of NlCYP6CS1 expression in the Sus, but the expression of NlCYP301B1 did not change significantly. In addition, RNA interference (RNAi)-mediated suppression of NlCYP6CS1 gene expression dramatically increased the toxicity of pymetrozine against N. lugens. Moreover, transgenic lines of Drosophila melanogaster expressing NlCYP6CS1 were less susceptible to pymetrozine, and had a stronger ability to metabolize pymetrozine. Taken together, our findings indicate that the overexpression of NlCYP6CS1 is one of the key factors contributing to pymetrozine resistance in N. lugens. And this result is helpful in proposing a management strategy for pymetrozine resistance.

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