Panonychus citri has developed resistance or cross-resistance to most registered acaricides; however, the molecular mechanism underlying acaricide cross-resistance remains to be elucidated. In this study, a field-collected population of P. citri was found to display high resistance to both abamectin and spirodiclofen (CoR-NN). A carboxyl/cholinesterase gene PcCCE11 is significantly upregulated in CoR-NN and after exposure to abamectin and spirodiclofen, respectively. Knockdown of PcCCE11 reduced CCEs hydrolytic activities and increased the sensitivity of P. citri to abamectin and spirodiclofen. Three-dimensional modeling and molecular docking analyses revealed that PcCCE11 can bind stably to abamectin and spirodiclofen. High-performance liquid chromatography and mass spectrometry analyses indicated that recombinant PcCCE11 can effectively degrade abamectin and spirodiclofen through hydrolysis. These results suggested that PcCCE11 is involved in the cross-resistance of P. citri to abamectin and spirodiclofen.
Keywords: Panonychus citri; abamectin; carboxyl/cholinesterases; cross-resistance; molecular mechanism; spirodiclofen.