Inheritance and biochemical mechanism of abamectin resistance in a near-isogenic strain of Panonychus citri (Acari: Tetranychidae).

The citrus red mite, Panonychus citri, has developed severe resistance to the widely used pesticide like abamectin. Understanding the inheritance, cross-resistance profile, and biochemical mechanism of pesticide resistance in P. citri is critical for developing effective resistance management strategies. Here, we established an abamectin-resistant near-isogenic strain (NIL-Aba) by backcrossing the susceptible strain (SS strain) with a field collected abamectin-resistant strain (NN-Aba strain) for eight generations, coupled with continuous abamectin selection. The NIL-Aba strain exhibited 2278.44-fold resistance to abamectin relative to the SS strain, and showed cross-resistance with high level to emamectin benzoate (2841.04-fold) and pyridaben (115.21-fold), moderate level to fenpropathrin (15.37-fold) and cyflumetofen (10.73-fold). Genetic analysis indicated that abamectin resistance in NIL-Aba was autosomal, polygenic, and incompletely recessive. Synergist and enzyme activity assays demonstrated that piperonyl butoxide and triphenyl phosphate significantly inhibited abamectin resistance, with synergism ratios of 2.42- and 2.57- fold, respectively. Diethyl maleate produced a smaller synergistic effect (SR = 1.60). Furthermore, the NIL-Aba strain exhibited significantly higher activities of cytochrome P450 monooxygenases, carboxylesterases and glutathione S-transferases than the SS strain, indicating the involvement of three enzyme families in abamectin detoxification. The establishment of NIL-Aba provides a genetically controlled resource for dissecting the molecular basis of abamectin resistance in P. citri. These findings also provide a theoretical foundation for rotating abamectin with other pesticides, which is crucial for prolonging its efficacy in the field against P. citri and for optimizing resistance management strategies.