Insect Biochemistry and Molecular Biology最新文献

The widespread emergence of resistance to diamide insecticides poses a significant threat to sustainable pest management. Rice, being one of the most important global staple crops, the emergence of insecticide resistance in key pests, poses a serious threat to food security and sustainable crop protection. This study investigates the mechanisms underlying resistance to chlorantraniliprole and flubendiamide in Cnaphalocrocis medinalis field populations. Bioassays revealed moderate to high levels of resistance for chlorantraniliprole (RR 71.75- to 1089.63-fold) and flubendiamide (RR 67.91- to 1572.64-fold). Synergism and biochemical assays indicated limited involvement of metabolic detoxification enzymes (Cyt, CarE, GST) in most resistant populations. Molecular characterization of the RyR gene identified multiple target-site mutations, including the novel I4712N substitution and a premature stop codon (Y4692*), as well as indications of gene duplication events. Notably, this study reports, for the first time, the field-evolved resistance to flubendiamide in C. medinalis globally. Our findings underscore the predominance of target-site-mediated resistance and highlight the need for functional validation of identified mutations. Continued monitoring, combined with molecular and genomic approaches, is crucial for guiding effective insecticide resistance management strategies in rice ecosystems.

Feeding regulation in Drosophila involves complex interactions between mechanosensory and neuroendocrine pathways. Our study identified transmembrane channel-like (TMC) as key regulators of crop size and contraction, functioning through distinct neuronal populations. They influence crop size via diuretic hormone, Dh44-expressing neuroendocrine cells in the pars intercerebralis (PI) region and regulate crop contraction through the serotonin receptor 5-HT7. We found that TMC is broadly expressed from the gut to the brain, reinforcing their role in the brain-gut axis. Mechanotransduction channels, including NompC, Piezo, and TMC, facilitate food ingestion, with TMC channels playing an additional role in food storage and transport. We noted the coexpression of piezo with Dh44 in only two neurons, indicating that at least two Dh44 cells are required for crop size regulation. Moreover, we identified Dh44R2 as the key receptor regulating crop size. Unlike DH44 and Piezo, TMC, 5-HT7, and TRPγ are essential for crop contraction, suggesting that these channels serve as therapeutic targets for regulating food intake. Our findings also support the involvement of a mechanosensory serotonergic pathway in regulating crop physiology, integrating sensory and neuroendocrine signals to control food storage and transport. These findings advance our understanding of the neuronal and molecular mechanisms underlying feeding behavior in Drosophila and provide a foundation for exploring conserved pathways that regulate food intake in other organisms, including mammals.

The ADAR family, which catalyzes adenosine-to-inosine (A-to-I) RNA editing on double-stranded RNA, represents an evolutionarily conserved RNA-modifying enzyme. While ADAR regulates microRNA (miRNA) maturation through both editing-dependent and -independent mechanisms, its role in organ development remains poorly characterized. In Bombyx mori, we previously identified high expression of BmADARa and BmSuc1 (encoding β-fructofuranosidase) in silk glands, with BmSuc1 known to regulate silk gland development. Here, we demonstrate that BmADARa controls silk gland patterning through miR-3315-BmSuc1 signaling axis. Specifically, we constructed RNAi-BmADARa mutants, and revealed that BmADARa is involved in regulating silk gland development and the expression levels of BmSuc1. Subsequent in-depth investigations demonstrated that BmADARa controls BmSuc1 expression by acting on its 3'UTR. Leveraging miRNA target prediction tools (miRanda and RNAhybrid), we identified miR-3315 as the exclusive candidate targeting the BmSuc1-3'UTR, with additional binding sites detected in the BmSuc1-CDS. BmADARa-RIP assays and Sanger sequencing provided conclusive evidence that BmADARa promotes miR-3315 maturation by editing pri-miR-3315. Moreover, KO-BmSuc1 mutants displayed altered expression patterns of sericin and fibroin genes, further validating that BmADARa regulates silk gland development through BmSUC1. In conclusion, our results show that BmADARa regulates the expression of BmSUC1, thereby positively influencing sericin gene expression in the anterior and middle silk glands and negatively regulating fibroin gene expression in the posterior silk gland. These results offer novel perspectives on the regulatory mechanisms governing silk gland development.

Spodoptera frugiperda is a major global pest that affect multiple crops, mainly corn and rice. Unfortunately, this pest has evolved resistance to various chemical and biological pesticides. ATP-binding cassette (ABC) transporters, particularly members of the B subfamily, are associated with detoxification by exporting xenobiotics and plant-derived metabolites from the intoxicated insect cells. In addition, some are involved in the mode of action of Bacillus thuringiensis biopesticide Cry toxins, functioning as receptors for these proteins. In this study, we analyzed transcriptomic data from the midgut tissue of S. frugiperda and identified the ABCB6 as one of the most highly expressed transporters within the ABCB subfamily. To explore its functional role, we generated a CRISPR-Cas9 knockout (KO) mutation. Strikingly, loss of SfABCB6 conferred resistance to the chemical pyrethroid insecticide cypermethrin, while the susceptibility to B. thuringiensis Cry1Ab, Cry1Fa and Vip3Aa toxins remained unchanged. Consistently, the ABCB6 CRISPR-Cas9 KO in S. frugiperda derived Sf9 cells conferred resistance to cypermethrin, reiterating the observed larval phenotype. In contrast, the overexpressing of ABCB6 in Sf9 cells exhibited increased susceptibility to cypermethrin. However, SfABCB6 KO showed fitness costs in the insect, as this mutation drastically reduced fertility. Our results provide evidence that SfABCB6 transporter facilitates cypermethrin toxicity participating in insecticide resistance and pointing out its potential role as a novel target for pest management strategies.

Juvenile hormones (JHs) play a crucial role in regulating development and reproduction in insects. In the cowpea aphid (Aphis craccivora), JH Ⅲ acid (JH ⅢA) can be converted into JH Ⅲ skipped bisepoxide (JHSB₃); however, the enzymes and pathways involved in this conversion remain elusive. In this study, we identified Ac-CYP6A14 as a key JH epoxidase and characterized its role in the JHSB₃ biosynthetic pathway in A. craccivora. In addition, we found that JHSB₃ titers were significantly higher in embryonic tissues than in maternal tissues. Transcriptomic analysis revealed six upregulated genes in the embryo. Temporal expression pattern analysis revealed that only Ac-CYP6A14 showed concordance with JHSB₃ titers. Silencing Ac-CYP6A14 decreased JHSB₃ titers. In vitro catalytic experiments demonstrated that Ac-CYP6A14 catalyzes the conversion of JH Ⅲ into JHSB₃. Furthermore, we found that the "epoxidation then esterification" sequence is not feasible. Collectively, our findings elucidated the JHSB₃ biosynthetic pathway, in which JH ⅢA is first esterified to form JH Ⅲ, followed by epoxidation to JHSB₃ by Ac-CYP6A14.

The ectoparasitic mite Varroa destructor is a major driver of honey bee mortality, yet its effects depend on the contrasting seasonal phenotypes of worker bees. We applied an integrated metabolomic and proteomic approach to dissect how Varroa parasitisation affects the molecular physiology of short-lived summer and long-lived winter bees. Newly generated summer data were integrated with a previously published winter dataset, enabling direct seasonal comparison under identical analytical pipelines. Season represented the dominant source of molecular variation; however, Varroa parasitisation elicited coherent but phenotype-dependent responses. In summer bees, parasitisation was associated with elevated post-emergence mortality and a pronounced metabolic shift characterised by altered purine turnover, membrane lipid remodelling and reduced tricarboxylic acid cycle throughput. These metabolomic changes were mirrored by proteomic changes in the abdomens indicative of stress-associated catabolism, mitochondrial dysfunction and reduced anabolic capacity. In contrast, winter bees exhibited limited metabolic plasticity but showed selective depletion of antioxidant enzymes, simple carbohydrates and nutritional proteins, consistent with impaired longevity-associated maintenance and nutrient allocation. Proteomic analysis of heads revealed a broader response than abdomens. In summer bee heads, Varroa parasitisation redirected investment towards membrane trafficking, transport and regulatory control at the expense of metabolic, sensory and secretory functions. Heads of Varroa-parasitised winter bees showed reduced abundance of immune, sensory and nutritional proteins, including vitellogenin. Our results demonstrate that V. destructor does not elicit a uniform stress response but exploits seasonally distinct physiological states of honey bees, generating divergent molecular stress patterns with direct implications for worker survival and colony resilience.