质膜H+-ATPase活性调节对于植物生长发育以及逆境胁迫适应十分重要。盐碱等逆境可以激活植物质膜H+-ATPase的活性，但是在非胁迫（正常）条件下其活性较低，处于“自抑制”状态。“自抑制”这一现象从发现至今已将近30年，但是其分子调控机制并不清楚。我们初步的实验发现，一个钙结合蛋白SCaBP3能够与质膜H+-ATPase AHA2 C端相互作用并抑制其活性，并且SCaBP3能够促进AHA2自身C端与胞质内大环的互作，同时，scabp3突变体具有耐受盐碱胁迫的表型。我们推测SCaBP3在植物质膜H+-ATPase活性“自抑制”状态的维持及盐碱胁迫响应中起了重要的作用。因此，本项目拟通过遗传、生理和生化等手段深入研究SCaBP3参与的质膜H+-ATPase活性调控的分子机制，阐明正常条件下质膜H+-ATPase活性“自抑制”状态维持的分子机制，以及盐碱胁迫下其“自抑制”状态解除的分子机制。

The regulation of plasma membrane H+-ATPase (PM H+-ATPase) activity is very important for plant growth and development and adaptation to stress. Saline-alkali stress can activate plant PM H+-ATPase activity, but under non-stress (normal) conditions, its activity is low and in an "autoinhibition" state. However, "autoinhibition" phenomenon has been discovered nearly 30 years, but its molecules regulatory mechanism is not clear yet. Our preliminary results indicated that a calcium-binding protein SCaBP3 interacts with the C-terminus of PM H+-ATPase AHA2 and inhibits its activity, and that SCaBP3 promotes the molecular interaction between the C-terminus of AHA2 and its intracytoplasmic macrocycles. Further, scabp3 mutant displays a resistant phenotype to saline-alkali stress. We speculate that SCaBP3 plays an important role in the maintaining "autoinhibition" state of PM H+-ATPase activity and the response of saline-alkali stress in plants. Therefore, this application intends to use genetic, physiological, and biochemical methods to further study the molecular mechanism of SCaBP3 involved in the regulation of PM H+-ATPase activity. We attempt to elucidate the molecular mechanism of "autoinhibition" state of PM H+-ATPase activity under normal conditions and the mechanism of release of its "autoinhibition" state under saline-alkali stress.