Abstract
Bemisia tabaci (Gennadius) is a serious agricultural pest worldwide. Neonicotinoids are the most important new class of synthetic insecticides used in the management of B. tabaci. However, B. tabaci populations have developed resistance to various active ingredients in neonicotinoids following long-term and widespread application.
Dinotefuran exhibited high toxicity against most B. tabaci field populations. One population (Din-R) with a high level of resistance to dinotefuran (255.6-fold) was first identified in the field. The Din-R population exhibited medium to high levels of resistance to all the tested neonicotinoid insecticides and a high level of resistance to spinetoram. Genetic inheritance analysis revealed that resistance to dinotefuran was incompletely recessive and polygenic. The synergist piperonyl butoxide significantly increased the toxicity of dinotefuran to Din-R. P450 activity in the Din-R population was 2.19-fold higher than in the susceptible population. RNA-sequencing analysis showed that 12 P450 genes were significantly upregulated in the Din-R population, of which CYP6DW5, CYP6JM1 and CYP306A1 were found to exhibit more than 3.00-fold higher expression in Din-R when using a reverse transcription quantitative real-time polymerase chain reaction. Expression of eight P450 genes was obviously induced by dinotefuran, and CYP6DW5 showed the highest expression level. After knockdown of CYP6DW5 in Din-R, the toxicity of dinotefuran increased significantly.
P450 had a crucial role in dinotefuran resistance in B. tabaci, and CYP6DW5 was involved in the resistance. These results provide important information for the management of resistance in B. tabaci and improve our understanding of the resistance mechanism of dinotefuran. © 2022 Society of Chemical Industry.
