摘要:

摘要: Spiders are an abundant group of natural enemies preying on insect pests in agroecosystem. But their potential in biological control has not been fully realized due to difficult mass production. One hindrance is the intense intraspecific aggression in spiders. Neurotransmitters such as serotonin play important roles in modulating aggression. Here, we investigated the regulatory function of serotonin (5-hydroxytryptamine [5-HT]) signaling in the intraspecific aggression in a wandering spider Pardosa pseudoannulata (Araneae, Lycosidae). The aggression was quantified with 5 escalated aggression behaviors as approach, chasing, lunging, boxing, and biting. Virgin (VG) females exhibited higher aggression levels but less 5-HT content than post-reproductive (PR) females. Systemic increase of 5-HT via 5-HT injection decreased aggression, while decrease of 5-HT via RNA interference (RNAi) of the tryptophan hydroxylase gene, increased aggression. The involvement of the four 5-HT receptors were determined via individual or combined RNAi. Co-RNAi of the three 5-HT1 genes increased overall aggression with decreased incidents of approach, chasing, lunging, and increased biting. RNAi of 5-HT1B decreased approach and increased biting, whereas RNAi of 5-HT1A or 5-HT1C did not affect aggression. RNAi of 5-HT7 decreased approach only. Therefore, different 5-HT receptor types contribute to different aspects of the inhibitory effects of 5-HT on aggression and provide several pharmacological targets for manipulating spider aggression. 5-HT injection did not affect spiders' predation on their insect prey, the brown planthopper Nilaparvata lugens. The findings reveal 1 neuronal mechanism regulating intraspecific aggression in spiders and provide an insight in developing aggression suppression strategies for spider mass rearing.

摘要: The adaptive strategies of prey against predation risk have been pivotal in non-consumptive effects. However, the adaptive strategies of prey and the response mechanisms to various predation risk cues remain unclear. We hypothesized that prey adopt a similar adaptive strategy to address different predation risks, but their response mechanisms depend on the attributes of predation risk cues. To test this hypothesis, we used Didinium-Paramecium as a predator-prey model to first evaluate the effects of various predation risk cues, including homogenates of predators (TD) and prey (TP) alone or in combination (TM), and the density of conspecific prey on the specific growth rate (SGR) to determine their adaptive strategies and their underlying response mechanisms based on transcriptomic analysis. Our results show that predation risk cues considerably enhance prey SGR, with effects in descending order of TM, TD, and TP. However, such effects gradually decrease as the density of conspecific prey increases until they disappear. The trend in the levels of differentially expressed genes (DEGs) in prey exposed to different predation risk cues is similar to that of SGRs. In particular, pathways based on DEG enrichment mediated by predation risk cues involve cellular processes, nutrient metabolism, and synthesis of biological macromolecules. However, they differ in type, number, and location within specific biological processes. In conclusion, Paramecium uses early reproduction strategies to address the risk of predation caused by different cues, and differences in its response mechanisms depend on the attributes of the cues of predation risk, resulting in differences in the SGR of the prey.

摘要: Pathological observations show that cancer cells frequently invade the surrounding normal tissue in collective rather than individual cell migration. However, general principles governing collective cell migration remain to be discovered. Different from individual cell migration, we demonstrated that the Notch-1-activation reduced collective cells speed and distances. In particular, Notch-1-activation induced cellular cytoskeletal remodelling, strengthened the intercellular junctions and cell-matrix adhesions. Mechanistically, Notch-1 activation prevented the phosphorylation of GSK-3 beta and the translocation of cytoplasmic free beta-catenin to the nucleus, which increased E-cadherin expression and tight intercellular junctions. Moreover, Notch-1 signalling also activated the RhoA/ROCK pathway, promoting reorganization of F-actin and contractile forces produced by myosin. Further, Notch-1 activation increased cell adhesion to the extracellular substrate, which inhibited collective cell migration. These findings highlight that cell adhesions and cell-cell junctions contribute to collective cell migration and provide new insights into mechanisms of the modulation of Notch-1 signalling pathway on cancer cell malignancy. Notch-1 activation (NICD) inhibits collective cell migration by promoting high intracellular force and strong cell-cell adhesion. Notch-1 activation leads to GSK-3 beta activity by inhibiting ILK phosphorylation, beta- catenin is degraded and cannot enter the nucleus, resulting in higher expression of E-cadherin and tighter intercellular connections. Additionally, Notch-1 stimulates the Rho/ROCK pathway, which enhances adhesions between cells and the extracellular matrix and ultimately impedes collective cell migration. image

摘要: Effective treatment of depression poses a major clinical challenge, accompanied by considerable social and emotional burdens. Electroacupuncture, a non-pharmacological modality derived from traditional Chinese medicine, offers a promising alternative for depression treatment due to its safety and efficacy. However, its underlying molecular mechanisms remain unclear. In this study, a corticosterone-induced depression model in C57BL/6 mice was employed and electroacupuncture was applied to stimulate at Zusanli (ST36) acupoint. The results demonstrated that electroacupuncture effectively alleviated depression-like symptoms and restored the structural morphology and plasticity of neurons in the hippocampal CA1 region. Further analysis revealed a significant upregulation of brain-derived neurotrophic factor (BDNF) and beta-type calmodulin-dependent protein kinase II (CaMKII beta), which are associated with neuronal plasticity regulatory pathways. This study elucidates the potential molecular mechanisms by which electroacupuncture alleviates depression through the regulation of neuroplasticity, providing an experimental basis for its clinical application.