Multiple Insecticide Resistance and Associated Metabolic-Based Mechanisms in a Myzus Persicae (Sulzer) Population

The green peach aphid, Myzus persicae (Sulzer) (Hemiptera: Aphididae), is an economically devastating crop pest worldwide. The M. persicae (SEF-R) population of a cabbage field in China was tested for susceptibilities to 13 insecticides. Compared with the susceptible population (FFJ-S), extremely high and high resistance to beta-cypermethrin (324-fold) and imidacloprid (106.9-fold) was detected in SEF-R. More importantly, this is the first report of resistance in the field M. persicae population to sulfoxaflor (32.4-fold), flupyradifurone (9.5-fold), pymetrozine (34.8-fold), spirotetramat (8.1-fold), flonicamid (5.8-fold), and broflanilide (15.8-fold) in China when compared with FFJ-S. The resistance factor decayed to a low level to sulfoxaflor and pymetrozine after 15 generations without any selection pressure. The resistance-related mutations (R81T and kdr) detected in SEF indicated target-site resistance to neonicotinoids and pyrethroids, respectively. Biochemical assays revealed the involvement of monooxygenase, carboxylesterase, superoxide dismutase, and peroxidase in a multi-insecticide resistance mechanism. The overexpression of P450s, esterases, and a UDP-glycosyltransferase might be responsible for the multi-insecticide resistance in SEF-R. The knockdown of CYP6CY3 in SEF-R increased its susceptibility to imidacloprid, thiacloprid, and thiamethoxam, which verified that P450s play vital roles in neonicotinoid metabolism. Our findings provide guidance for the rational use of insecticides to delay resistance development in GPA.

Automated summary

This study investigated the resistance of the green peach aphid to 13 insecticides in a cabbage field in China. The results showed that the aphids had high resistance to beta-cypermethrin and imidacloprid, and this is the first report of resistance to sulfoxaflor, flupyradifurone, pymetrozine, spirotetramat, flonicamid, and broflanilide in China. The resistance is associated with target-site mutations and overexpression of enzymes. The findings provide guidance for the rational use of insecticides to delay resistance development.