Functional roles of nicotinic acetylcholine receptors in dinotefuran and flupyrimin toxicity and their sublethal effects on Sogatella furcifera (Hemiptera: Delphacidae).

Abstract

Sogatella furcifera (Horváth) (Hemiptera: Delphacidae), a serious rice pest, has developed significant resistance to a wide range of pesticides. Neonicotinoid insecticides are currently the primary choice for controlling S. furcifera, yet their impact on the species remains poorly understood. In this study, we investigated the binding sites of a conventional insecticide (dinotefuran) and a novel insecticide (flupyrimin), and evaluated their sublethal effects on S. furcifera. Our results revealed that the LC50 of dinotefuran and flupyrimin were 2.51 mg/L and 2.80 mg/L in third-instar S. furcifera, respectively. RNA interference (RNAi) knockdown of S. furcifera nicotinic acetylcholine receptor (nAChR) alpha2 subunit (Sfα2) and S. furcifera nAChR beta1 subunit (Sfβ1) significantly reduced the susceptibility to dinotefuran by 18.7% and 16.8%, respectively, but had no effect on flupyrimin. Reproduction of the F0 and F1 generations was significantly inhibited by the LC25 of both dinotefuran and flupyrimin. In the dinotefuran treatment at LC25, the intrinsic growth rate (r) and finite growth rate (λ) were reduced to 0.15 and 0.16 days, respectively; the mean generation time (T) increased to 27.77 days, and the relative fitness was only 0.76 compared to the control. Additionally, the relative fitness (Rf) of the flupyrimin-treated group was reduced to 0.93 and 0.86 times that of the control group. The population dynamics of S. furcifera are significantly affected by both dinotefuran and flupyrimin, making these insecticides valuable tools for integrated pest management and the rational use of insecticides.