Regulation and physiological integration of salt stress signaling and adaptation in Arabidopsis

盐分胁迫是一种主要的非生物胁迫，表现为土壤中钠离子浓度升高，对植物生长和作物产量产生不利影响。植物发展了复杂的机制来感知和适应这种压力。植物盐分感知和适应的核心是所谓的盐过度敏感(SOS)途径。在这里，钙传感器SOS3/CBL4可能破译了盐胁迫诱导的钙信号，并在直接相互作用时激活了激酶SOS2/CIPK24。因此，这种钙传感器-激酶复合体激活了H/Na逆向转运体SOS1，以促进钠的排出。在Na胁迫的背景下，钙信号的出现以及通过AHA-PM ATPase对pH动态平衡和H通量的适应性调节已经被很好地记录下来。然而，这些H泵是如何调节的，以及它们是如何与SOS途径相互连接的，仍有待研究。此外，虽然已经描述了耐盐性的核心途径，但很明显，它需要与所有其他植物调节电路和信号网络密切相连和整合。然而，这种互联互通的要素才刚刚开始出现。在我们的初步工作中，两位申请人都认识到在盐胁迫期间形成的钙模式的巨大复杂性，确定了SOS2/CIPK24与不同的钙传感器之间的替代相互作用作为盐响应中的调节开关，发现SOS2/CIPK24的多重磷酸化是SOS途径的可能整合机制，并确定了CBLS/CIPKs与AHA2 H泵之间的直接调控相互作用。根据我们的初步数据，该项目的主要目标是：1.分析盐诱导的从细胞到组织水平的钙信号，并表征其功能及其与其他信号系统的相互作用。2.蛋白-蛋白相互作用、转磷酸化及其与其他信号转导过程的整合对蛋白激酶SOS2的调节。通过调节SOS途径鉴定和鉴定与耐盐性有关的新成分。通过结合我们的反向遗传资源、新建立的报告系和互补的专业知识，并结合细胞生物学方法和体内分子表型分析，我们打算识别关键成分，并表征介导植物盐胁迫反应与植物发育可塑性和生理动态平衡整合的基本分子机制。

Salt stress in form of elevated sodium (Na+) concentrations in the soil is a major abiotic stress which adversely affects plant growth and crop yield. Plants developed elaborate mechanisms to sense and adapt to this stress. Central to plant salinity sensing and adaptation is the so called salt overly sensitive (SOS) pathway. Here, the calcium sensor SOS3/CBL4 likely deciphers salt stress induced Ca2+ signals and activates the kinase SOS2/CIPK24 upon direct interaction. Consequently, this Ca2+ sensor-kinase complex activates the H+/Na+ antiporter SOS1 for Na+ extrusion. In the context of Na+ stress the occurrence of Ca2+ signals and the adaptive regulation of pH homeostasis and H+ fluxes via AHA-PM ATPases have been well documented. However, how these H+ pumps are regulated and how they are interconnected with the SOS pathway remains to be investigated. Moreover, while the core-pathway for salt tolerance has been described it is obvious that it needs to be intimately interconnected and integrated with all other plant regulatory circuits and signaling networks. However, elements of this interconnection are only beginning to emerge. In our preliminary work, both applicants recognized an enormous complexity of Ca2+ patterns that are formed during salt stress, identified alternative interactions of SOS2/CIPK24 with distinct Ca2+ sensors as regulatory switches in salt responses, uncovered multiple phosphorylation of SOS2/CIPK24 as a likely integration mechanism for the SOS pathway and identified direct regulatory interactions between CBLs/CIPKs with the AHA2 H+ pump. Based on our preliminary data the proposed project specifically aims to address:1. The analysis of salt induced Ca2+ signals from the cellular to the organismic level and the characterization of their function and interconnection with other signaling systems. 2. The regulation of the kinase SOS2 by protein-protein interactions and transphosphorylation and its integration with other signaling processes.3. The identification and characterization of novel components contributing to salt tolerance by modulating the SOS pathway.4. The investigation of components interconnecting Ca2+ signaling and regulating AHA H+-ATPase activity for proton/pH regulation in plant salt tolerance By combining our reverse-genetic resources, newly generated reporter lines and complementary expertise and by using a combination of cell-biological approaches and in vivo molecular phenotype analyses, we intend to identify critical components and to characterize fundamental molecular mechanisms that mediate the integration of plant salt stress responses with plant developmental plasticity and physiological homeostasis.