环境温度对动物的衰老速率有着重要影响。模式动物中的研究表明，在生命早期经历适度的环境高温可以延长寿命。其部分原因是高温激活PMK-1通路，并通过表观遗传调控持续提升机体的基础免疫。然而动物根据环境温度而适应性调整基础免疫的机制还远未得到深入系统的解释。申请者前期利用秀丽隐杆线虫研究发现，与基础免疫密切相关的核糖体生物合成（RiBi）受到高温显著影响，大量与RiBi相关的基因被抑制表达，表明其可能参与高温对基础免疫的影响。据此，本项目拟主要从以下两个方面深入研究RiBi在其中的功能和机制：（1）阐明RiBi在环境温度调节基础免疫和衰老速率中的功能；（2）研究RiBi与PMK-1通路以及温度相关的表观遗传调控因子之间的作用关系。本研究可进一步揭示RiBi的生理功能，并从机制上加深对环境温度、基础免疫和衰老调控之间关系的认识，为从环境温度影响基础免疫的角度实现抵抗衰老具有重要的理论指导意义。

Environmental temperature has substantial effects on the aging rate of animals. Early life exposure to mild high environmental temperature can extend the lifespan of some model organisms. The genetics underlying the longevity response to hormetic high temperature are confirmed by activating the PMK-1 pathway, which in turn triggers the epigenetic regulations, to promote long-lasting basal innate immune responses. However, the detailed mechanisms for animals to adjust their basal immunity to environmental temperature remain unclear. By using C. elegans as model organism, we found that ribosome biogenesis (RiBi), which is essential to innate immunity, was affected by ambient temperature. Almost all of the RiBi genes were inhibited at high temperature, indicating that RiBi would be involved in the basal immune responses activated by high temperature. Based on these findings, this project aims to study the critical roles for RiBi in temperature-induced basal immune activation. We will focus on two aspects: (1) elucidate the critical roles of RiBi in basal immune activation and longevity induced by high temperature; (2) examine the interaction between RiBi and PMK-1 pathway，and analyze the interaction between RiBi and temperature-related epigenetic factors. Our project would reveal novel physiological function of RiBi, and deepen our understanding of the relationship of environmental temperature, innate immunity and aging process. This project would provide mechanistic insights into how hormetic high temperature promotes longevity by activating basal immune responses.