Emamectin benzoate inhibits growth and development of Hyphantria cunea, accompanied by disruptions in lipid metabolism and hormonal balance

Abstract

To clarify the physiological effects of low-concentration emamectin benzoate (EMB) exposure, its sublethal and semi-lethal impacts on Hyphantria cunea growth and development were evaluated. Initially, the 72 h LC₂₀ (0.021 mg/L) and LC₅₀ (0.032 mg/L) of EMB against 4th instar larvae were determined using the leaf-dip method. Short-term observations following treatment with these concentrations revealed significant inhibition of larval growth and food utilization efficiency. Long-term observations revealed that EMB treatment significantly inhibited larval and pupal development, reduced pupation and adult emergence rates, and shortened adult longevity, resulting in successful development rates of only 22.42 % (LC₂₀) and 1.83 % (LC₅₀). Transcriptomic analysis, qRT-PCR, and biochemical assays further demonstrated that short-term treatment (72 h on the 4th instar) upregulated genes related to lipid metabolism (HcLipase, HcGK, HcDES9, HcAGPAT, and HcFAR) and significantly reduced triacylglycerol (TAG) levels. Long-term treatment (24 h exposure followed by rearing to the 7th instar) led to transcriptional suppression of these genes and continued TAG depletion. Nile red staining confirmed reduced lipid droplet size in fat bodies, indicating impaired lipid storage. Additionally, EMB disrupted hormonal homeostasis in both 4th- and 7th-instar larvae, as evidenced by the downregulation of HcJHEH and upregulation of HcJHR, leading to increased juvenile hormone levels. Conversely, genes related to 20-hydroxyecdysone (20E) (HcCYP306A1, HcCYP314A1, HcCYP18A1, and HcEcR) were significantly downregulated, accompanied by a significant decrease in 20E titers. In conclusion, this study revealed the potential mechanism of EMB action, whereby it inhibits the growth and development of H. cunea by disrupting lipid metabolism and hormonal balance.