The fall armyworm, Spodoptera frugiperda, is an invasive agricultural pest that is a serious threat to agricultural production and global food security. Chemical control is the most effective method for preventing outbreaks of S. frugiperda. However, insecticide resistance often develops as a result of prolonged pesticide use, and the molecular mechanisms involved in insecticide resistance remain unclear. Insect cytochrome P450 monooxygenases play an important role in the detoxification of insecticides and insecticide resistance in Lepidoptera. In our study, the LC₅₀ of a novel insecticide (cyproflanilide) and a conventional insecticide (emamectin benzoate) for S. frugiperda second-instar larvae were 7.04 and 1.61 mg/L, respectively. Furthermore, CYP321A9 expression was upregulated in larvae exposed to these insecticides. Additionally, knockdown of CYP321A9 by feeding larvae with dsRNA for 72 h significantly increased the mortality of S. frugiperda exposed to emamectin benzoate and cyproflanilide by 23.33% and 7.78%, respectively. Our results indicate that CYP321A9 may play an important role in the detoxification of emamectin benzoate and cyproflanilide in S. frugiperda. Our findings provide a basis to better understand the mechanisms of insecticide resistance and contribute to the control of S. frugiperda.

Graphical Abstract