肝肠胞虫（EHP）调控Toll-Rap2a抑制凡纳滨对虾生长的分子机制

对虾是我国水产养殖的重要种类，肝肠胞虫（Enterocytozoon hepatopenaei，EHP）是养殖对虾的主要病原，感染导致对虾生长缓慢甚至停滞，已严重制约我国对虾产业发展。针对肝肠胞虫通过先天性免疫Toll途径调控生长关键基因Rap2a影响对虾生长这一科学问题，本项目拟重点开展以下研究：（1）EHP感染对对虾Toll途径的影响，（2）Toll途径抑制Rap2a表达的分子机制，（3）Rap2a对对虾生长的调控机制及（4）EHP通过Toll-Rap2a介导对虾生长抑制机制。通过探究对虾Toll免疫通路与对虾生长的关系，阐明Toll激活抑制Rap2a表达，为免疫调控生长提供新的途径，揭示EHP引起对虾生长抑制的分子机制，为深入研究不同病原刺激下免疫通路与生长代谢之间相互作用提供借鉴，也对对虾养殖过程中病害防控策略的制定提供理论依据。

Shrimps occupy a predominant position in China aquaculture industry. Enterocytozoon hepatopenaei (EHP), one of the most severe threats to cultivated shrimp worldwide, inhibiting the growth of shrimp, seriously restricted the development of shrimp industry in China. In recent years, the relationship between immunity and growth has become a research hot spot in various species, especially in economic animals. However, the relationship between immunity and growth of shrimps is still unclear, and the mechanism of pathogens causing growth inhibition in prawn remains to be explored. Based on the scientific problem that how EHP regulated growth-related gene Rap2a through the innate immune Toll pathway to affect the growth of prawn, this project focused on the following studies: a. the effect of EHP infection on the Toll pathway activation of Litopenaeus vannamei; b. the molecular mechanism of LvToll inhibiting LvRap2a via LvDorsal; c. the regulation of LvRap2a on shrimp growth; d. the molecular mechanism of EHP inhibiting the growth of shrimp by via LvToll4-LvRap2a. Elucidating the molecular mechanism of Toll4-Rap2a-mediated growth inhibition in shrimp reveals the mechanism of growth inhibition in shrimps after EHP infection. The results of this project will for the first time linking the activation of innate immune pathway to the shrimp growth. It will lay a foundation for the further development of the interaction between immune pathway and growth metabolism under different pathogen stimuli, and will also of great significance for the development of disease control plan in shrimp culture.