Mutations of the complex I PSST target gene confers acaricide resistance and a fitness cost in Panonychus citri.

BACKGROUND

Pesticide resistance is a serious problem that threatens crop industries. Major resistance towards pyridaben, an acaricidal inhibitor of mitochondrial electron transport complex I (METI-Is), has been reported in tetranychids following its extensive use worldwide. Understanding mechanisms of pyridaben resistance is crucial for sustainable resistance management.

RESULTS

The inheritance of pyridaben resistance was incompletely recessive and controlled by multiple genes in P. citri, which was determined by reciprocal crosses and backcross experiments. Bulked segregant analysis was performed to identify gene loci underlying pyridaben resistance. Subsequently, the two PSST-subunit mutations H107R and the previously undiscovered V103I mutation were positively correlated with pyridaben resistance in different populations or strains by single mite genotyping. The bioassay further showed that H107R contributed to moderate resistance, while V103I in combination with H107R was responsible for a very high level of resistance in homozygous P. citri strains. These contributions to pyridaben resistance were also verified in transgenic Drosophila through the introduction of the wildtype, single- or double-mutated P. citri PSST subunit. In addition, life-table analysis and behavioral measures were conducted to assess the fitness cost associated with resistance development. Accompanied by reduced ATP levels and complex I activity, a fitness cost was observed as reduced fecundity and lower mobility due to PSST mutations.

CONCLUSIONS

Our findings provide direct evidence that PSST mutations conferred the evolution of pyridaben resistance but simultaneously led to a fitness cost due to functional defects in complex I. These data provide theoretical insights into sustainable resistance management in agricultural production.