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Bemisia tabaci is one of the most destructive agricultural insect pests around the world, and it has developed high levels of resistance to most pesticides. Dimpropyridaz, a novel insecticide developed by BASF, displays excellent activity against piercing-sucking insect pests. In this study, baseline of susceptibility showed all tested field populations of B. tabaci are susceptible to dimpropyridaz. After continuous selection with dimpropyridaz in the lab, a B. tabaci strain (F12) developed 2.2-fold higher level of resistance compared with a susceptible MED-S strain, and the realized heritability (h 2) was estimated as 0.0518. The F12 strain displayed little cross-resistance to afidopyropen, cyantraniliprole, sulfoxaflor, or abamectin, and significantly increased activity of cytochrome P450 monooxygenase (P450). The fitness cost of dimpropyridaz resistance was evident in F12 strain, which had a relative fitness of 0.95 and significantly lower fecundity per female compared with MED-S strain. Taken together, B. tabaci displays high susceptibility to dimpropyridaz in the field, and low risk of developing resistance to dimpropyridaz under successive selection pressure. Little cross-resistance to popular insecticides was found, and fitness cost associated dimpropyridaz resistance was observed. Higher activity of cytochrome P450 in the F12 strain, may be involved in the process of detoxifying dimpropyridaz in whitefly. [Display omitted] • All tested field populations of Bemisia tabaci are highly susceptible to dimpropyridaz. • B. tabaci displays low risk to dimpropyridaz after continuous selections. • Dimpropyridaz showed little cross-resistance to the selected popular insecticides. • Cytochrome P450 monooxygenase could be involved in detoxification of dimpropyridaz. • Dimpropyridaz-resistance conferred fitness cost in the F12 strain of B. tabaci. [ABSTRACT FROM AUTHOR]

Bemisia tabaci is a formidable insect pest worldwide, and it exhibits significant resistance to various insecticides. Dimpropyridaz is a novel pyridazine pyrazolecarboxamide insecticide used against sucking insect pests, but there is little information regarding its metabolic detoxification in arthropods or cross-resistance with other insecticides. In this study, we found that dimpropyridaz shows no cross-resistance with three other popular insecticides, namely abamectin, cyantraniliprole, and flupyradifurone. After treatment of B. tabaci adults with a high dose of dimpropyridaz, higher cytochrome P450 monooxygenase (P450) activity was detected in the survivors, and the expression of the P450 gene CYP6DW4 was highly induced. Cloning and characterization of the full-length amino acid sequence of CYP6DW4 indicated that it contains conserved domains typical of P450 genes, phylogenetic analysis revealed that it was closely related to a B. tabaci protein, CYP6DW3 , known to be involved in detoxification of imidacloprid. Silencing of CYP6DW4 by feeding insects with dsRNA significantly increased the susceptibility of B. tabaci to dimpropyridaz. In addition, homology modeling and molecular docking analyses showed the stable binding of dimpropyridaz to CYP6DW4 , with binding free energy of −6.65 kcal/mol. Our findings indicate that CYP6DW4 plays an important role in detoxification of dimpropyridaz and possibly promotes development of resistance in B. tabaci. [Display omitted] • Dimpropyridaz showed no cross-resistance to abamectin, cyantraniliprole, flupyradifurone. • High-dose selection of dimpropyridaz highly induced activity of P450 monooxygenase. • Knockdown of CYP6DW4 greatly increased mortality of B. tabaci to dimpropyridaz. • Dimpropyridaz could stably bind to CYP6DW4 in molecular docking. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]