病毒在感染细胞的过程中可以引发宿主细胞的细胞骨架微管和微丝的重新排列，使之有利于病毒的侵入及其在细胞内的运输。但是，这里面的具体分子机制还不清楚。在本项目前期的研究中，我们发现含有RCC1结构域蛋白超家族中的新成员RCCD1对细胞骨架的重塑具有非常重要的调控作用。敲低RCCD1的表达，不仅可以改变细胞骨架微管的稳定性，还会引发微丝的剧烈重排。因此，本申请项目拟以正链RNA病毒EMCV和负链RNA病毒VSV为研究对象，系统研究RCCD1及其结合蛋白JIP4在RNA病毒感染过程中的功能，并深入研究RCCD1-JIP4相互作用在RNA病毒感染引起的宿主细胞骨架重排中的调控机制。进而利用活性荧光染料对活病毒进行标记，并研究RCCD1-JIP4相互作用对于病毒沿细胞骨架侵入及其胞内运输过程的调控机制进行深入探索。本项目研究结果将进一步加深我们对于RNA病毒感染细胞的侵入和转运过程的分子机制的认识。

In the process of infection, virus can trigger the rearrangement of cytoskeletal microtubules and microfilaments in host cells, making it more suitable for its entry and intracellular trafficking. However, the detailed molecular mechanism of this process is still largely unclear. Our preliminary data suggested that RCCD1, a new member of the RCC1 domain superfamily, plays an important role in regulating the remodeling of cell cytoskeleton. By siRNA transfection, we found that depletion of RCCD1 not only changed the stability of microtubules, but also caused a violent rearrangement of the microfilaments. Thus, we propose that RCCD1 may play an important role in virus infection. In this project, we intend to study the function of RCCD1 and its binding protein JIP4 in the process of RNA virus infection by using EMCV and VSV. We will further investigate the impact and molecular mechanism of RCCD1-JIP4 interaction on RNA virus induced cytoskeletal reorganization in host cells. Then live virus will be labeled with fluorescent dyes. The process of virus entry and its intracellular trafficking along the cytoskeleton in RCCD1/JIP4 depleted- or overexpressed- cells will be intensively explored. These studies will deepen our understanding of the molecular mechanisms involved in the entry and intracellular trafficking of RNA virus.