SOS1 is a key systemic regulator of salt secretion and K+/Na+ homeostasis in the recretohalophyte Karelinia caspia
SOS1 is a key systemic regulator of salt secretion and K+/Na+ homeostasis in the recretohalophyte Karelinia caspia
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DOI：
10.1016/j.envexpbot.2020.104098
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发表时间：
2020-09-01
影响因子：
5.7
通讯作者：
Mur, Luis A. J.
中科院分区：
文献类型：
--
作者：
Guo, Qiang;Meng, Lin;Mur, Luis A. J.
在高盐条件下，海葵（kalelinia caspia）最重要的适应策略之一是通过盐腺分泌过量的盐到叶片表面，以维持K+/Na+的稳态。质膜Na+/H+反转运蛋白（SOS1）参与Na+转运，并与糖细胞的K+营养相关。然而，尚不清楚这种适应策略是否与天牛的SOS1有关。在这里，我们探讨了KcSOS1的可能作用。KcSOS1定位于质膜，其表达受盐的调控和诱导。KcSOS1在拟南芥sos1突变体中的表达恢复了其耐盐性，表明KcSOS1是一种Na+外排蛋白。利用RNA干扰技术，在盐胁迫下生长受到严重影响的赤豆中产生kcsos1沉默系。KcSOS1的沉默破坏了Na+转运系统，导致在200 mM NaCl存在下，与野生型相比，KSLs的Na+分泌率降低。由于根木质部液对K+的净吸收较低，ksl的K+积累也有所下降。KcHKT1、KcNHX1和KcPHA，或KcAKT1、KcAKT2和KcSKOR等与K+/Na+稳态相关的质子泵、Na+转运体或K+通道编码基因的表达在KSLs的不同组织中下调。综上所述，我们的研究结果表明KcSOS1通过调节Na+转运参与盐的分泌过程，并间接调节K+的摄取/转运。这些机制维持了系统的K+/Na+稳态，从而赋予耐盐性。
One of the most important adaptive strategies is the secretion by salt glands of excessive salt to the leaf surface to maintain K+/Na+ homeostasis in the recretohalophyte Karelinia caspia under high salt conditions. The plasma membrane Na+/H+ antiporter (SOS1) has been shown to be involved in Na+ transport and correlated with K+ nutrition in glycophytes. However, it remains unclear whether this adaptive strategy is associated with SOS1 in K. caspia. Here, we explored the possible role of KcSOS1. KcSOS1 was localized to the plasma membrane, and its expression was regulated and induced by salt. Expression of KcSOS1 in an Arabidopsis sos1 mutant restored its salt tolerance, indicating that KcSOS1 is a Na+ efflux protein. RNA interference was used to generate KcSOS1-silenced-lines (KSLs) in K. caspia that the growth was severely affected by salt. Silencing KcSOS1 disrupted the Na+ transport system, resulting in decreased Na+ secretion rates in KSLs compared to that in wild-type in the presence of 200 mM NaCl. KSLs also displayed a decline in K+ accumulation resulting from low net K+ uptake into the root-xylem-sap. The expression of genes encoding proton pump, Na+ transporters or K+ channels linked to K+/Na+ homeostasis, including KcHKT1, KcNHX1 and KcPHA, or KcAKT1, KcAKT2 and KcSKOR, was downregulated in different tissues of KSLs. Overall, our findings suggest that KcSOS1 participates in the process of salt secretion by regulating the Na+ transport, and also indirectly modulates the K+ uptake/transport. These mechanisms maintain systemic K+/Na+ homeostasis to confer salt tolerance.