关于光致盐胁迫水稻(Oryza sativa L.)Na+离子流逆转机制的研究

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.

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。

水稻是一种盐敏感作物，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，但植物对外部光和盐浓度的综合机制目前还不清楚。在本研究中，我们证明光照增强了无盐和NaCl处理水稻根部的阳离子(Na+、K+、H+和Ca2+)外排，但NaCl处理水稻在光照状态下Na+、J(Na+)净通量相反。这种倒置的光诱导J(Na+)信号表明盐胁迫和光信号之间存在交替串扰，盐胁迫通过下调光受体干扰Na+的转运。蛋白质-蛋白质相互作用网络显示，桥接组和AKT1钾通道存在光敏色素(phychrome, PHY) A、B、光促素(PHOT) 1A、1B和2，桥接组和阳离子转运组界面存在价阳离子/H+反转运蛋白和Na+/K+反转运蛋白(SOS1)。接下来差异表达基因分析显示，10 mM NaCl处理7天以上，茎部光受体无显著变化(Log2(FC)< 0.5)，根部OsHKT2、1m OsHKT1;5、AKT1和AKT2 (Log2(FC) < -2, p-value < 0.01)均显著下调。虽然SOS1没有显著的表达变化(Log2(FC) < 0.5)，但盐胁迫诱导的抗氧化下调会干扰质膜H+泵，如阳离子/H+反转运蛋白(CHX17)，将Na+信号逆转到光。此外，我们利用STORM超分辨成像可视化Na+选择性通道OsHKT2;1和SOS1的表达分布。结果表明，NaCl刺激组将这些跨膜通道分散在细胞质和质膜上，而无盐组沿质膜分布良好。最后，Ca2+介导的Na+信号的初步理论模型显示J(Na+)随着外部[NaCl]的增加而降低。为改进模型，提出了含H+介质的交替理论模型。这种独特的倒置光诱导J(Na+)开关为理解盐胁迫和光信号之间的相互作用提供了一种新的范式。