SOS1, HKT1;5, and NHX1 Synergistically Modulate Na(+) Homeostasis in the Halophytic Grass Puccinellia tenuiflora.
SOS1, HKT1;5, and NHX1 Synergistically Modulate Na(+) Homeostasis in the Halophytic Grass Puccinellia tenuiflora.
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DOI：
10.3389/fpls.2017.00576
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发表时间：
2017
影响因子：
5.6
通讯作者：
Wang SM
中科院分区：
文献类型：
--
作者：
Zhang WD;Wang P;Bao Z;Ma Q;Duan LJ;Bao AK;Zhang JL;Wang SM
星星草是一种典型的耐盐型盐生草，具有优良的耐盐性。质膜Na+/H+转运蛋白SOS 1、HKT型蛋白和液泡膜Na+/H+逆向转运蛋白NHX 1是植物耐盐性的关键Na+转运蛋白。本研究在前期研究的基础上，根据盐胁迫下星星草中PtSOS 1的表达和Na+、K+水平的变化，提出了这些转运蛋白在Na+稳态中的功能模型。在这里，我们分析了PtSOS 1，PtHKT 1;5，和PtNHX 1的表达模式，在细花紫菜在25和150 mM NaCl下，结合以前的生理特性，进一步验证这个模型。结果表明，在25和150 mM NaCl胁迫下，PtSOS 1和PtHKT 1;5在根中的表达均被诱导，并在6 h达到高峰。与对照相比，在25 mM NaCl胁迫下，PtSOS 1的表达量增加了5.8倍，而PtHKT 1;5的表达量仅增加了1.2倍;相反，在150 mM NaCl胁迫下，PtSOS 1的表达量增加了1.4倍，而PtHKT 1;5的表达量增加了2.2倍。此外，PtNHX 1诱导瞬时下25 mM NaCl，而其表达更高，更持久的芽下150 mM NaCl。这些结果为先前的假设提供了更强有力的证据，并扩展了模型，该模型强调SOS 1，HKT 1;5和NHX 1协同调节Na+稳态，通过控制Na+运输系统在整个植物水平在低盐和高盐条件下。在轻度盐胁迫下，PtNHX 1将Na+缓慢地分隔到液泡中，液泡对Na+的潜在隔离能力通过反馈调节，增强PtSOS 1向根木质部的Na+负载，从而使Na+通过蒸腾流从根向地上部转运，进行渗透调节。而在高盐胁迫下，PtNHX 1能迅速将Na+固定到叶肉细胞的液泡中，使液泡对Na+的固定能力达到饱和，从而调节Na+从根向地上部的远距离运输。结果表明，PtHKT 1;5的表达被强烈诱导，从而使过量的Na+从木质部卸载到木质部薄壁细胞中。
Puccinellia tenuiflora is a typical salt-excluding halophytic grass with excellent salt tolerance. Plasma membrane Na+/H+ transporter SOS1, HKT-type protein and tonoplast Na+/H+ antiporter NHX1 are key Na+ transporters involved in plant salt tolerance. Based on our previous research, we had proposed a function model for these transporters in Na+ homeostasis according to the expression of PtSOS1 and Na+, K+ levels in P. tenuiflora responding to salt stress. Here, we analyzed the expression patterns of PtSOS1, PtHKT1;5, and PtNHX1 in P. tenuiflora under 25 and 150 mM NaCl to further validate this model by combining previous physiological characteristics. Results showed that the expressions of PtSOS1 and PtHKT1;5 in roots were significantly induced and peaked at 6 h under both 25 and 150 mM NaCl. Compared to the control, the expression of PtSOS1 significantly increased by 5.8-folds, while that of PtHKT1;5 increased only by 1.2-folds in roots under 25 mM NaCl; on the contrary, the expression of PtSOS1 increased by 1.4-folds, whereas that of PtHKT1;5 increased by 2.2-folds in roots under 150 mM NaCl. In addition, PtNHX1 was induced instantaneously under 25 mM NaCl, while its expression was much higher and more persistent in shoots under 150 mM NaCl. These results provide stronger evidences for the previous hypothesis and extend the model which highlights that SOS1, HKT1;5, and NHX1 synergistically regulate Na+ homeostasis by controlling Na+ transport systems at the whole-plant level under both lower and higher salt conditions. Under mild salinity, PtNHX1 in shoots compartmentalized Na+ into vacuole slowly, and vacuole potential capacity for sequestering Na+ would enhance Na+ loading into the xylem of roots by PtSOS1 through feedback regulation; and consequently, Na+ could be transported from roots to shoots by transpiration stream for osmotic adjustment. While under severe salinity, Na+ was rapidly sequestrated into vacuoles of mesophyll cells by PtNHX1 and the vacuole capacity became saturated for sequestering more Na+, which in turn regulated long-distance Na+ transport from roots to shoots. As a result, the expression of PtHKT1;5 was strongly induced so that the excessive Na+ was unloaded from xylem into xylem parenchyma cells by PtHKT1;5.