Myosin Va和KIF3A通过介导mTOR和MAPK信号通路调控中华绒螯蟹血淋巴-精巢屏障结构的形成

动物精子发生的安全性是生殖生物学的热点领域，支持细胞与生精细胞之间的互作是其核心问题。申请人前期研究发现，十足目甲壳动物精巢中存在血淋巴-精巢屏障，其中桥粒和黏附连接是一屏障的两个重要结构。但迄今我们对虾蟹类的血淋巴-精巢屏障形成的动力学机制知之甚少。已知Kinesin和Myosin在桥粒（Dsc2）和黏附连接（N-cadherin）关键因子转运中发挥动力学作用。我们拟研究中华绒螯蟹血淋巴-精巢屏障形成及功能实现中的动力机制。用离体和活体干扰、活细胞成像及蛋白功能分析技术等，研究KIF3A和Myosin Va在血淋巴-精巢屏障形成中的动力学，试图揭示两种马达蛋白通过参与Dsc2和N-cadherin转运并调控mTOR和MAPK信号通路维持血淋巴-精巢屏障的结构完整性及功能实现。本研究将开拓甲壳动物生殖生物学研究领域，填补甲壳动物精子发生安全性以及精子质量控制的空白。

The safety of spermatogenesis is one of the hot topics nowadays. The mutual interaction between Sertoli cells and spermatogenic cells is one of the main key questions. In our previous studies, the applicant and his collaborators/partners had found that, in the decapod crustaceans, there exists hemolymph-testis barrier. Desmosome and septate junction are two of the main structures in this barrier. Unfortunately, nobody knows how this barrier is formed. Nevertheless the molecular dynamic mechanisms of the formation of hemolymph-testis barrier. In mammalian, there are at least two kinds of motor proteins participate in the formation of desmosome and septate junction. Kinesin and Myosin transport Dsc2 and N-cadherin, which helps the construction of desmosome and septate junction. We speculate that, in the decapod crustaceans, there exists similar pathway which regulates the genesis of junctional complex in testis. In this project, we will focus on KIF3A and Myosin Va. These two motors had been found in testis of Chinese mitten crab. We have also detected N-cadherin in the testis in this species, which is the main component of septate junction. We doubt that KIF3A and Myosin Va are involved in the construction of junctional complex in the testis. We try to reveal the molecular mechanism of the security of crustacean spermatogenesis by this project.