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

拟南芥盐胁迫信号传导和适应的调节和生理整合

• 批准号: 410758888
• 负责人: Professor Dr. Jörg Kudla
• 金额: --
• 依托单位: National Natural Science Foundation of China
• 依托单位国家: 德国
• 项目类别: Research Grants
• 财政年份: 2019
• 资助国家: 德国
• 起止时间: 2018-12-31 至 2021-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/410758888?language=en
• 关键词: Regulation; physiological; integration; salt; stress

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.

盐胁迫是一种主要的非生物胁迫，其形式为土壤中钠（Na+）浓度升高，这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。植物盐敏感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SOS 3/CBL 4可能破译盐胁迫诱导的Ca 2+信号，并在直接相互作用时激活激酶SOS 2/CIPK 24。因此，这种Ca 2+传感器-激酶复合物激活H+/Na+反向转运蛋白SOS 1以进行Na+排出。在Na+胁迫的背景下，Ca 2+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被充分证明。然而，这些H+泵是如何调节的，以及它们如何与SOS通路相互联系，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互连和整合。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，两个申请人都认识到盐胁迫期间形成的Ca 2+模式的巨大复杂性，鉴定了SOS 2/CIPK 24与不同Ca 2+传感器的替代相互作用作为盐响应中的调节开关，揭示了SOS 2/CIPK 24的多重磷酸化作为SOS途径的可能整合机制，并鉴定了CBL/CIPK与AHA 2 H+泵之间的直接调节相互作用。根据我们的初步数据，拟议项目的具体目标是解决：1。从细胞水平到器官水平分析盐诱导的Ca ~（2+）信号，并对其功能和与其他信号系统的相互关系进行表征。2.激酶SOS 2通过蛋白-蛋白相互作用和转磷酸化的调节及其与其他信号传导过程的整合.通过SOS途径调控植物耐盐性的新组分的鉴定和表征.植物耐盐性中Ca ~（2+）信号和AHA H ~+-ATP酶活性相关组分的研究通过结合我们的反向遗传资源、新产生的报告基因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，我们打算确定关键成分，并表征介导植物盐胁迫反应与植物发育可塑性和生理功能整合的基本分子机制。体内平衡