Abstract
The brown planthopper, Nilaparvata lugens, is an economically important pest on rice in Asia. Chemical control is still the most efficient primary way for rice planthopper control. However, due to the intensive use of insecticides to control this pest over many years, resistance to most of the classes of chemical insecticides has been reported. In this article, we report on the status of eight insecticides resistance in Nilaparvata lugens (Stål) collected from China over the period 2012–2016. All of the field populations collected in 2016 had developed extremely high resistance to imidacloprid, thiamethoxam, and buprofezin. Synergism tests showed that piperonyl butoxide (PBO) produced a high synergism of imidacloprid, thiamethoxam, and buprofezin effects in the three field populations, YA2016, HX2016, and YC2016. Functional studies using both double-strand RNA (dsRNA)-mediated knockdown in the expression of CYP6ER1 and transgenic expression of CYP6ER1 in Drosophila melanogaster showed that CYP6ER1 confers imidacloprid, thiamethoxam and buprofezin resistance. These results will be beneficial for effective insecticide resistance management strategies to prevent or delay the development of insecticide resistance in brown planthopper populations.
Highlights
The brown planthopper (BPH), Nilaparvata lugens (Stål) (Hemiptera: Delphacidae), is a serious pest on rice in Asia[1]
Our results indicated that N. lugens have developed high resistance levels to imidacloprid, buprofezin, thiamethoxam, pymetrozine and flufiprole, a medium resistance level to chlorpyrifos
The results showed that resistance levels of six insecticides imidacloprid, thiamethoxam, nitenpyram, sulfoxaflor, buprofezin and flufiprole have a dramatic increase in 2015 and 2016 compared with former three years (Supplementary Table S4 and Fig. 2) and previously reported[6,24]
Summary
The brown planthopper (BPH), Nilaparvata lugens (Stål) (Hemiptera: Delphacidae), is a serious pest on rice in Asia[1]. It was generally accepted that, changes in detoxifying enzymes, especially enhanced cytochrome P450 monooxygenase (P450) activity contributes to the neonicotinoid resistance of field-collected populations of BPH5,15–19. This detoxification mechanism was initially implicated by use of the metabolic enzyme inhibitor piperonyl butoxide (PBO) and the model substrate 7-ethoxycoumarin[13,14]. The aim of this study was to provide the changing levels of resistance to eight insecticides in N. lugens field strains collected from eight provinces in China from 2012 to 2016, and to study the relative roles of the cytochrome P450 monooxygenase (P450), CYP6ER1 and CYP6AY1, in determining their resistance phenotype to imidacloprid, thiamethoxam and buprofezin
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