BACKGROUND: Fall armyworm (FAW, Spodoptera frugiperda) is one of the most destructive and invasive pests worldwide and causes significant economic losses. Intensive and frequent use of insecticides has led to the development of resistance in FAW. Adipokinetic hormone (AKH) have been proven to be involved in insecticide resistance in insects. However, the molecular mechanism underlying chlorantraniliprole resistance mediated by AKH signaling in FAW remains unclear.RESULTS: The expression of SpfAKHR was highest in male adults and lowest in 1st instar larvae. SpfAKH was expressed the highest in eggs and the lowest in 6th instar larvae. AKH signaling was involved in the sensitivity of FAW to chlorantraniliprole through a toxicological bioassay, and the combination of chlorantraniliprole and bithionol (an inhibitor of key enzymes in the AKH pathway) significantly increased the mortality of FAW. Chlorantraniliprole significantly induced the expression of ten P450s, SpfAKH and SpfAKHR in FAW. RNA interference against SpfAKHR significantly decreased the P450 content, downregulated the expression of three P450 genes (SpfCYP6B50, SpfCYP321A9 and SpfCYP9A58) and inhibited the resistance of FAW to chlorantraniliprole. The topical application of AKH peptide significantly increased the P450 content, upregulated the expression of five P450 genes (SpfCYP321A9, SpfCY321A8, SpfCYP321A10, SpfCYP321A7 and SpfCYP6AB12), and enhanced the survival of FAW against chlorantraniliprole.CONCLUSIONS: AKH plays an important role in enhancing chlorantraniliprole resistance in FAW by exerting a positive influence on P450 gene expression and P450 content. These results provide valuable insights into insecticide resistance regulation and FAW control strategies.
Juvenile hormones (JHs) play a crucial role in the development of honey bee (Apis mellifera) worker larvae. Juvenile hormone analogs (JHAs), insecticides widely used in pest control, have been reported to affect the health and survival of honey bee worker larvae. However, the molecular mechanisms of JHAs in the honey bee remain unclear. In this study, we treated honey bee worker larvae with pyriproxyfen, fenoxycarb, and methoprene, three different JHAs. We monitored the changes in the transcription of genes encoding major JH response enzymes (CYP15A1, CYP6AS5, JHAMT, and CHT1) using RT-qPCR and analyzed the transcriptome changes in worker larvae under JHA stress using RNA-seq. We found that the enrichment pathways differed among the treatment groups, but the classification of each pathway was generally the same, and fenoxycarb affected more genes and more pathways than did the other two JHAs. Notably, treatment with different JHAs in the honey bee changed the JH titers in the insect to various extents. These results represent the first assessment of the effects of three different JHAs on honey bee larvae and provide a new perspective and molecular basis for the research of JH regulation and JHA toxicity in the honey bee.
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