Mutations in the GSTe2 Promoter in the Emamectin Benzoate-Resistant Strain of Spodoptera frugiperda Contribute to Elevated Expression Levels and Enhanced Metabolic Detoxification Capacity against Emamectin Benzoate.

While emamectin benzoate (EB) remains a key insecticide against Spodoptera frugiperda, significant resistance has developed, compromising its effectiveness. Identifying response genes and mutations is critical for resistance management. Here, genome resequencing and transcriptome analysis of EB-resistant (EB-R) and EB-susceptible (EB-Sus) strains of S. frugiperda identified 177 candidate genes. Subsequently, four glutathione S-transferase (GST) genes, one Cytochrome P450 gene, and one ABC gene linked to insecticide resistance were selected for functional validation. Among these, GSTe2 was highlighted for its most upregulated and high EB affinity. Injection with dsGSTe2 increased the larval mortality by 28.3% under EB stress. UPLC-MS/MS confirmed that GSTe2 metabolizes EB in vitro. Crucially, three single-nucleotide polymorphisms in the GSTe2 promoter (EB-R) enhanced its transcriptional activity. Collectively, we propose a resistance mechanism: promoter mutations elevate GSTe2 transcription and metabolic capacity for EB. This research provides a foundation for targeted insecticidal strategies using key resistance genes, thereby enhancing the efficacy of pest control measures.