从细胞学的角度研究植物响应盐胁迫的分子机制具有重要的意义。微丝骨架的组织和稳定性的动态变化对于盐胁迫下植物的存活是重要的，然而微丝在其中的作用机制、参与该过程的微丝结合蛋白及其调控机理有待深入研究。申请人课题组前期在拟南芥中鉴定到微丝封端蛋白capping protein (CP,包括CPA和CPB两个亚基)参与了植物响应盐胁迫的生理学过程，且CPA与Na+/H+反向转运体SOS1相互作用。在此基础上，本项目拟着重探讨CP在植物细胞响应盐胁迫中的作用机理以及与SOS1的互作关系。通过细胞生物学等手段对盐胁迫下CP调控微丝的功能，参与拟南芥细胞响应盐胁迫的机理，特别是盐胁迫下CPA与SOS1互作的特征及生理学意义等进行研究。本项目将着重解决微丝封端蛋白CP参与SOS1介导的植物响应盐胁迫的具体机制，为深入认识微丝骨架参与植物响应非生物逆境的作用机理提供重要的理论依据。

It is important to understand the molecular mechanisms of plant response to salt stress from the cell biology point of view. Dynamic organization and instability of actin filaments is crucial for plant survival under salt stress. However, the function of actin binding proteins involved in these processes and their regulatory mechanisms in plant response to salt stress remain largely unclear. The applicant functionally identified the Arabidopsis actin capping protein (CP, containing two subunits CPA and CPB) as participants in plant response to salt stress. Moreover, CPA interacts with the Na+/H+ antiporter SOS1. Based on these preliminary results, the applicant proposes to investigate the physiological functions and cellular mechanisms of CP involved in plant response to salt stress. The molecular mechanisms of CP that regulates actin filaments and subsequently affects seedling growth and survival under salt stress will be investigated. In particular, the applicant will study the characteristics of CPA interacting with SOS1 and the physiological functions of their interaction in plant response to salt stress. This research will unravel the mechanism as to how actin filaments participate in SOS1-mediated plant acclimation to salt stress through CP, which provides new knowledge to understand how actin filaments function in plant cells in response to abiotic stress.