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.