Characterization of abamectin resistance in <i>Grapholita molesta</i> (Lepidoptera: Tortricidae): cross-resistance, inheritance, fitness costs, and biochemical mechanisms

The oriental fruit moth, Grapholita molesta (Busck) (Lepidoptera: Tortricidae), is a globally significant pest of fruit crops. Its management has long relied on abamectin, yet resistance evolution threatens its effectiveness. In this study, a laboratory relative susceptible strain (AM-S) was subjected to 19 consecutive generations of selection with abamectin, resulting in a resistant strain (AM-R) showing a 132.5-fold increase in LD50. The AM-R strain displayed significant cross-resistance to emamectin benzoate (43.8-fold), imidacloprid (16.5-fold), but little to no cross-resistance to lambda-cyhalothrin, bifenthrin, thiamethoxam, or chlorpyrifos. Genetic analyses indicated that abamectin resistance was autosomal, incompletely dominant (D = 0.11-0.30), and polygenic, as shown by significant deviations from monogenic inheritance in backcross tests. Resistance incurred substantial fitness costs, including extended larval and pupal durations, reduced larval and pupal weights (by 20-25%), lower fecundity (1.45-fold fewer eggs), and shortened adult longevity. Synergism assays revealed that piperonyl butoxide (SR = 2.87) and diethyl maleate (SR = 2.23) significantly enhanced abamectin toxicity, and biochemical assays showed 3.65-fold higher cytochrome P450 and 2.75-fold higher glutathione S-transferase activities in the resistant strain, implicating metabolic detoxification as the major mechanism. These results demonstrate that abamectin resistance in G. molesta evolves rapidly under continuous exposure, is polyfactorial and metabolically mediated, and imposes measurable biological trade-offs. Together, these insights clarify how physiological trade-offs and metabolic adaptation shape abamectin resistance in G. molesta, informing longer-term strategies for more sustainable pest management systems.