Computational Insights into the Different Resistance Mechanism of Imidacloprid versus Dinotefuran in Bemisia tabaci

Abstract

Insecticide resistance is a critical problem for pest control and management. For Bemisia tabaci, striking high metabolic resistance (generally conferred by CYP6CM1) was observed for imidacloprid (IMI) and most other neonicotinoid members. However, dinotefuran (DIN) displayed very low resistance factors, which indicated distinct metabolic properties. Here, molecular modeling methods were applied to explore the different resistance features of IMI versus DIN within the Q type of CYP6CM1. It was found that Arg225 played crucial roles in the binding of IMI-CYP6CM1vQ with a cation-π interaction and two stable H-bonds; however, such interactions were all absent in the DIN-CYP6CM1vQ system. The stable binding of IMI with CYP6CM1vQ would facilitate the following metabolic reaction, while the weak binding of DIN might disable its potential metabolism, which should be an important factor for their distinct resistance levels. The findings might facilitate future design of the antiresistance neonicotinoid molecules.

Differential metabolism of neonicotinoids by <i>Myzus persicae</i> CYP6CY3 stably expressed in <i>Drosophila</i> S2 cells

“…2B), indicating that M. persicae with imidacloprid resistance obtained by the overexpression of CYP6CY3 will not show strong resistance to dinotefuran. As is the case of B. tabaci CYP6CM1, 12) it is possible that the binding of dinotefuran to CYP6CY3 is weak. Thus, the lack of metabolism of dinotefuran explains why the FCR strain has the same level of resistance against dinotefuran and sulfoxaflor.…”

Characterization of flupyradifurone resistance in the whitefly Bemisia tabaci Mediterranean (Q biotype)

“…17,18 In B. tabaci, CYP6CM1 was shown to be highly associated with resistance to pymetrozine and imidacloprid, 19,20 and CYP6CM1vQ conferred distinct levels of resistance to dinotefuran and imidacloprid. 21 Recently, CYP4CS3, CYP4C64, CYP6CX2, CYP6CX4, CYP6CX5, CYP6DW2, and CYP6DW3 were linked to neonicotinoid insecticide resistance. 22,23 Similarly, GSTs also have an important role in the detoxification of several classes of insecticides such as organophosphate, pyrethroid, and neonicotinoid insecticides.…”

Susceptibility of Bemisia tabaci MEAM1 (Hemiptera: Aleyrodidae) to Imidacloprid, Thiamethoxam, Dinotefuran and Flupyradifurone in South Florida

“…Flupyradifurone (Sivanto 200 SL) first became commercially available for use in Florida vegetables in 2015, shortly after the last populations in this study were collected from the field. Flupyradifurone possesses the same mode of action as the neonicotinoid insecticides, but like dinotefuran, is not detoxified by the microsomal monooxygenases, including the P450 gene CYP6CM1, that have been implicated in the development of resistance to imidacloprid and other neonicotinoid insecticides by B. tabaci [24,31,32]. Nauen et al [31] demonstrated that flupyradifurone lacks metabolic cross-resistance to imidacloprid.…”