ROS-Mediated COXI Overexpression by AMPKα Confers Resistance to Dimefluthrin and Cross-Resistance to Indoxacarb in Aedes albopictus

Increased electron respiratory chain complex and Na+, K+-ATPase activity, ROS content, COXI and AMPKα expression, and decreased free ATP content were detected in a dimefluthrin-resistant Aedes albopictus (Ae. albopictus) strain established in laboratory, which developed high-level resistance to dimefluthrin and cross-resistance to indoxacarb and the resistance ratio of 21.61- and 62.14-fold shifted to 8.69- and 8.00-fold to dimefluthrin and indoxacarb after silencing COXI. When silencing AMPKα, the ROS content increased by 1.74 times and the expression of COXI was decreased by 59.00%, leading to a significant increase in the susceptibility of resistant Ae. albopictus to dimefluthrin. Removing ROS by N-acetylcysteine remarkably decreased the expression of AalAMPKα, restored the expression of COXI, and significantly increased the mortality of resistant Ae. albopictus when exposed to dimefluthrin and indoxacarb, suggesting that COXI played a crucial role in mediating the resistance to dimefluthrin and indoxacarb by modulating AalAMPKα expression. The study showed that dimefluthrin triggered the outbreak of ROS, subsequently modulated the expression of COXI, and as a result induced the AalAMPKα-mediated resistance to insecticides targeted voltage-gated sodium channel.