Abstract
Bemisia tabaci is a formidable insect pest worldwide, and exhibits significant resistance to various insecticides. Flupyradifurone is one novel butenolide insecticide and has emerged as a new weapon against B. tabaci, but field-evolved resistance to this insecticide has become a widespread concern. To unravel the mechanisms of field-evolved flupyradifurone resistance, we conducted a comprehensive investigation into susceptibility of twenty-one field populations within the Beijing-Tianjin-Hebei Region of China. Alarmingly, thirteen of these populations displayed varying degrees of resistance, ranging from low to medium levels, and building upon our prior findings, we meticulously cloned and characterized the CYP6CX4 gene in B. tabaci. Our investigations unequivocally confirmed the association between CYP6CX4 overexpression and flupyradifurone resistance in three of the thirteen resistant strains via RNA interference. To further validate our findings, we introduced CYP6CX4 overexpression into a transgenic Drosophila melanogaster line, resulting in a significant development of resistance to flupyradifurone in D. melanogaster. Additionally, homology modeling and molecular docking analyses showed the stable binding of flupyradifurone to CYP6CX4, with binding free energy of -6.72 kcal mol[-1]. Collectively, our findings indicate that the induction of CYP6CX4 exerts one important role in detoxification of flupyradifurone, thereby promoting development of resistance in B. tabaci.
