Abstract
Heavy metals are prevalent environmental contaminants in pest habitats. This study investigates the tolerance of Hyphantria cunea larvae to β-cypermethrin under cadmium (Cd) stress. Exposure to Cd markedly enhanced larval tolerance to β-cypermethrin. The P450 enzyme was found to be crucial in triggering this cross-tolerance. Notably, Cd exposure significantly upregulated the expression of HcCYP333A29 and HcCYP6AE184 both before and after β-cypermethrin treatment. Silencing these genes reduced the β-cypermethrin tolerance in Cd-exposed larvae. Furthermore, overexpression of HcCYP333A29 and HcCYP6AE184 significantly improved the tolerance of Sf9 cells and Drosophila to β-cypermethrin. Silencing of HcDicer-1, a key gene in the miRNA synthesis pathway, significantly diminished the β-cypermethrin tolerance in Cd-treated larvae. The miR-2739 controlled overexpression of HcCYP333A29, while miR-2854 controlled HcCYP6AE184 overexpression, both of which were essential for β-cypermethrin cross-tolerance in H. cunea larvae under Cd exposure. Collectively, Cd exposure induces cross-tolerance to β-cypermethrin in H. cunea larvae through miRNA-mediated post-transcriptional regulation.
