水稻是盐敏感农作物，土壤盐化是影响水稻产量的关键不利因素。光对植物生长发育起着有益作用。植物对外部光和盐浓度的综合机制还不清楚。我们拟研究盐胁迫和光刺激之间的信号相互作用，了解有益的光信号是如何转换高盐给植物带来的负面影响。为了研究光对盐胁迫的影响，我们初步研究了水稻根部的实时光刺激诱导的离子流出信号(Na+，K+，H+，Cl-和Ca2+)与外部盐浓度的关系。结果显示，光照使盐胁迫的水稻根部除Na+外的其它净阳离子流出量增多。为了在分子水平上研究新发现的Na+信号反转机制，本项目从信号分析、转录组分析和蛋白质组分析等方面进行研究。此外，通过对Na+排出起主要作用的SOS和电压门控离子通道和水通量进行实时检测来研究盐胁迫作用对离子稳态和水稳态的破坏影响。最后建立理论模型并进行计算机模拟以确认我们的研究观点和结果。本项新发现对了解高盐对盐敏感水稻产生的破坏机制和建立恢复机制至关重要。

Rice is used as the food for about half of the world’s population. Because it is a salt-sensitive crop, salinity is a major negative constraint to rice production, while light is a major positivity in plant growth and development. How plants integrate the external light and salinity signals remains poor understandings. To get the insights to compensate this negatively affected salt stress-induced signals with a positively affected physical light condition, here, we proposed the study of the integrated switchable signals of salt stress and light stimuli. The real-time light-inducible ion efflux signals, J(Na+), J(K+), J(H+), J(Cl-) and J(Ca2+), from the rice root would be related with the external salt stress. Our preliminary works showed in general that net effluxes of cations of the NaCl-treated rice were enhanced by light exposure, except J(Na+). This new finding would be a critical clue to understand the damaging mechanism from the salt-stress for the salt-sensitive plants, like rice (Oryza sativa L.). This unique reversed mechanism of J(Na+) has to be confirmed, characterized, and identified down to the molecular level. Therefore, this work will be included the study of signal analysis, the transcriptomic analysis, and proteomic analysis. In addition, temporal disruption of salt stress in ion and water homeostasis will be studied by choosing the key players of Na+ extrusion channels (SOS and voltage-gated ion channel) and water flux Theoretical model will be built, and computational simulation will be performed for confirming. This unique study of a light-inducible ionic switch for rice will be a cornerstone for building a possible compensating mechanism for salt-damaging mechanism.