RESUMO
Various plant species contain terpene secondary metabolites, which disrupt insect growth and development by affecting the activity of juvenile hormone-degrading enzymes, and the juvenile hormone (JH) titers maintained in insects. Nerolidol, a natural sesquiterpenol belonging to the terpenoid group, exhibits structural similarities to insect JHs. However, the impact of nerolidol on insect growth and development, as well as its underlying molecular mechanism, remains unclear. Here, the effects of nerolidol on Spodoptera exigua were investigated under treatment at various sub-lethal doses (4.0 mg/mL, 1.0 mg/mL, 0.25 mg/mL). We found that a higher dose (4.0 mg/mL) of nerolidol significantly impaired the normal growth, development, and population reproduction of S. exigua, although a relatively lower dose (0.25 mg/mL) of nerolidol had no significant effect on this growth and development. Combined transcriptome sequencing and gene family analysis further revealed that four juvenile hormone esterase (JHE)-family genes that are involved in juvenile hormone degradation were significantly altered in S. exigua larvae after nerolidol treatment (4.0 mg/mL). Interestingly, the juvenile hormone esterase-like (JHEL) gene Sexi006721, a critical element responsive to nerolidol stress, was closely linked with the significant augmentation of JHE activity and JH titer in S. exigua (R2 = 0.94, p < 0.01). Taken together, we speculate that nerolidol can function as an analog of JH by modulating the expression of the enzyme genes responsible for degrading JH, resulting in JH disorders and ultimately disrupting the development of insect larvae. This study ultimately provides a theoretical basis for the sustainable control of S. exigua in the field whilst proposing a new perspective for the development of novel biological pesticides.
Assuntos
Sesquiterpenos , Animais , Spodoptera/genética , Sesquiterpenos/farmacologia , Terpenos/farmacologia , Insetos , Hormônios Juvenis/farmacologiaRESUMO
The (E)-ß-farnesene (EßF) is one of the most important secondary metabolites in some plants and provides indirect defense against aphids. However, the direct effect of EßF against pests is still unclear. In this study, various concentrations of EßF (0.16, 0.8, and 4 g/kg) were provided in an artificial diet to determine the direct effects of EßF on Spodoptera exigua. The results showed that an artificial diet containing 4 g/kg of EßF 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 EßF bioassay in an artificial diet also indicated that the proliferation of the S. exigua population was inhibited by the ingestion of EßF 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 EßF at a dose of 0.8 and 4 g/kg when compared with two controls (p < 0.05). This indicated that EßF 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 EßF at the larval stage, relative to the expression of these genes after treatment with controls. These findings suggested that EßF 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.
RESUMO
Evolution of resistance by pests has diminished the efficacy of transgenic crops producing insecticidal proteins from Bacillus thuringiensis (Bt). In China, where transgenic cotton producing Bt toxin Cry1Ac has been planted since 1997, field control failures have not been reported but the frequency of resistance to Cry1Ac has increased in the cotton bollworm, Helicoverpa armigera. This provides incentive to switch to multi-toxin Bt cotton, which is grown in many other countries. Previous work created four laboratory strains of H. armigera with >100-fold resistance to Cry1Ac, with the genetic basis of resistance known in all but the LF256 strain. Here, we analyzed the genetic basis of resistance in Cry1Ac in LF256 and evaluated cross-resistance of all four strains to three toxins produced by widely planted multi-toxin Bt cotton: Cry1Fa, Cry2Ab, and Vip3Aa. DNA sequencing revealed that LF256 lacked the mutations in three genes (HaTSPAN1, HaABCC2, and HaABCC3) that confer resistance to Cry1Ac in two other strains of H. armigera we analyzed. Together with previous results, the data reported here show that each of the four strains examined has a different genetic basis of resistance to Cry1Ac. Significant positive cross-resistance occurred to Cry1Fa in three of the four strains tested but not to Cry2Ab or Vip3Aa in any strain. Thus, Cry2Ab and Vip3Aa are likely to be especially valuable for increasing the efficacy and durability of Bt cotton against H. armigera populations that have some resistance to Cry1Ac.
RESUMO
Pectinophora gossypiella (Lepidoptera: Gelechiidae) is a key pest in many cotton-growing countries of the world. In this study, the complete mitochondrial (mt) genome of the pink bollworm P. gossypiella was determined, which is 15,202 bp in length (GenBank accession number: KM225795) containing 37 typical animal mitochondrial gene and an A + T-rich region. The gene order of P. gossypiella mtDNA was different from the insect ancestral gene order in the translocation of trnM, as shared by previously sequenced lepidopteran mtDNAs. The protein-coding genes (PCGs) have typical mitochondrial start codons ATN, with the exception of COI, Nad5, which uses the start codons CGA, GTT. Eight PCGs stop with complete termination codons (TAA), whereas five PCGs use incomplete stop codon T. All of the tRNA genes had typical cloverleaf secondary structures except for trnS1(AGN), in which the dihydrouridine (DHU) arm did not form a stable stem-loop structure. Like other insects, the control region is located between rrnS and trnM with a length of 309 bp and an A + T content of 94.8%, which is the most AT-rich region and comparatively simple, with little evidence of long tandem repeats, but harbors a conserved structure combining the motif ATAGA and a 18-bp poly-T stretch.
