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

盐胁迫是土壤中钠（Na+）浓度升高的一种主要非生物胁迫，对植物生长和作物产量产生不利影响。植物发展出复杂的机制来感知和适应这种压力。植物盐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可能破译盐胁迫诱导的Ca2+信号，并通过直接相互作用激活SOS2/CIPK24激酶。因此，这种Ca2+传感器激酶复合物激活了H+/Na+反转运蛋白SOS1，用于Na+挤压。在Na+胁迫下，Ca2+信号的发生以及通过AHA-PM atp酶对pH稳态和H+通量的适应性调节已经得到了很好的证明。然而，这些氢离子泵是如何调节的，以及它们如何与SOS通路相互连接，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紧密相连和整合。然而，这种相互联系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盐胁迫期间形成的Ca2+模式的巨大复杂性，确定了SOS2/CIPK24与不同Ca2+传感器的替代相互作用作为盐反应的调节开关，揭示了SOS2/CIPK24的多重磷酸化可能是SOS通路的整合机制，并确定了CBLs/CIPKs与AHA2 H+泵之间的直接调节相互作用。根据我们的初步数据，提议的项目具体旨在解决：1。盐诱导Ca2+信号从细胞到机体水平的分析及其功能表征和与其他信号系统的互连。2. 蛋白-蛋白相互作用和转磷酸化对SOS2激酶的调控及其与其他信号过程的整合。3 .通过调节SOS通路促进耐盐性的新组分的鉴定和表征。通过结合我们的反向遗传资源，新生成的报告系和互补专业知识，并通过结合细胞生物学方法和体内分子表型分析，研究连接Ca2+信号和调节AHA H+- atp酶活性的成分对植物耐盐性中质子/pH调节的影响。本研究旨在确定植物盐胁迫响应与植物发育可塑性和生理稳态整合的关键成分和基本分子机制。

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.