The F116V mutation and overexpression of CYP9A186 confer high-level resistance to emamectin benzoate and abamectin in Spodoptera exigua.

The beet armyworm, Spodoptera exigua, is a polyphagous, migratory pest of worldwide importance. It has developed serious resistance to emamectin benzoate and abamectin due to the widespread use of these insecticides in pest control. Previous research demonstrated that the F116V mutation in CYP9A186 confers 265-fold resistance to emamectin benzoate (EB) and 45-fold resistance to abamectin in the WH-EB strain of S. exigua, a near-isogenic strain obtained by introgression of field resistance into the susceptible WH-S line via repeated backcrossing. Here, we examine the contribution of CYP9A186 in a 2024 field population from Alaer, Xinjiang, China (named ALE24), in which the F116V mutation is fixed. The F116V allele from ALE24 was introgressed into the susceptible WH-S strain through repeated backcrossing, yielding a near-isogenic strain (WH-ALE). WH-ALE exhibited 1286-fold resistance to EB and 300-fold resistance to abamectin, which is approximately 5 times greater than that of WH-EB for each respective insecticide. In addition, WH-ALE showed low levels of cross-resistance (2.8- to 4.7-fold) to indoxacarb, esfenvalerate, spinosad, chlorpyrifos, and chlorantraniliprole, but no cross-resistance to chlorfenapyr or broflanilide. Importantly, WH-ALE showed dramatically elevated expression of the mutant CYP9A186 allele, with a 72.9-fold increase in the midgut and a 56.8-fold increase in the fat body relative to the WH-S strain, indicating strong metabolic amplification. These results demonstrate that high-level resistance to EB and abamectin in WH-ALE is conferred by the combined effects of the F116V substitution and its marked overexpression. Therefore, resistance monitoring programs should assess both the presence and expression levels of specific resistance alleles of CYP9A186 in S. exigua populations to improve adaptive resistance management.