The main component of the aphid alarm pheromone (E)-beta-farnesene affects the growth and development of Spodoptera exigua by mediating juvenile hormone-related genes

The (E)-beta-farnesene (E beta F) is one of the most important secondary metabolites in some plants and provides indirect defense against aphids. However, the direct effect of E beta F against pests is still unclear. In this study, various concentrations of E beta F (0.16, 0.8, and 4 g/kg) were provided in an artificial diet to determine the direct effects of E beta F on Spodoptera exigua. The results showed that an artificial diet containing 4 g/kg of E beta F reduced the final survival of the S. exigua larvae and per female fecundity of adults significantly when compared with CK and SC controls (p < 0.05), then ultimately it also significantly affected the intrinsic rate of increase (p < 0.05). Furthermore, the results of the E beta F bioassay in an artificial diet also indicated that the proliferation of the S. exigua population was inhibited by the ingestion of E beta F in a dose-dependent manner. Combined differential RNA-seq data and RT-qPCR analysis, it was found that four key genes involved in juvenile hormone degradation significantly upregulated in S. exigua larvae treated by E beta F at a dose of 0.8 and 4 g/kg when compared with two controls (p < 0.05). This indicated that E beta F could disturb the normal function of juvenile hormones and reduce the survival rate of S. exigua larvae. Additionally, two key genes that regulate per fecundity of S. exigua females, including SeVg and SeVgR, were significantly downregulated in adult females (p < 0.05) when they were treated with 0.8 and 4 g/kg of E beta F at the larval stage, relative to the expression of these genes after treatment with controls. These findings suggested that E beta F first disturbed the normal function of juvenile hormone by upregulating key degradation genes, and then inhibited the expression of SeVg/SeVgR genes and proteins, thus reducing the population size of S. exigua by increasing larval mortality and inhibiting per female fecundity.