Molecular Mechanism Underlying ROS-Mediated AKH Resistance to Imidacloprid in Whitefly.

Simple Summary: As an invasive pest, whitefly causes great losses in agricultural production, and resistance increases in whitefly to chemical insecticides are an important problem in plant protection. Our study revealed that imidacloprid stress inhibits the expression of AKH, thereby increasing ROS and the expression levels of the resistance gene CYP6CM1 and upstream regulatory factors in Bemisia tabaci. AKH silencing by RNA interference affected the resistance of whiteflies to imidacloprid. These results provide insight into the resistance mechanism in whitefly. Synthetic insecticides used to control Bemisia tabaci include organophosphorus, pyrethroids, insect growth regulators, nicotinoids, and neonicotinoids. Among these, neonicotinoids have been used continuously, which has led to the emergence of high-level resistance to this class of chemical insecticides in the whitefly, making whitefly management difficult. The adipokinetic hormone gene (AKH) and reactive oxygen species (ROS) play roles in the development of insect resistance. Therefore, the roles of AKH and ROS in imidacloprid resistance in Bemisia tabaci Mediterranean (MED; formerly biotype Q) were evaluated in this study. The expression level of AKH in resistant B. tabaci MED was significantly lower than that in sensitive B. tabaci (MED) (p < 0.05). AKH expression showed a decreasing trend. After AKH silencing by RNAi, we found that ROS levels as well as the expression levels of the resistance gene CYP6CM1 and its upstream regulatory factors CREB, ERK, and P38 increased significantly (p < 0.05); additionally, whitefly resistance to imidacloprid increased and mortality decreased (p < 0.001). These results suggest that AKH regulates the expression of resistance genes via ROS in Bemisia tabaci. [ABSTRACT FROM AUTHOR]