SOS1 is a key systemic regulator of salt secretion and K+/Na+ homeostasis in the recretohalophyte Karelinia caspia

文献类型： 外文期刊

第一作者： Guo, Qiang

作者： Guo, Qiang;Meng, Lin;Mao, Peichun;Tian, Xiaoxia;Zheng, Mingli;Han, Jiwan;Mur, Luis A. J.;Mur, Luis A. J.

作者机构：

关键词： Recretohalophyte; Karelinia caspia; SOS1; Ion transporters; K+/Na(+)homeostasis; Salt secretion; Salinity

期刊名称：ENVIRONMENTAL AND EXPERIMENTAL BOTANY （ 影响因子：5.545； 五年影响因子：5.99 ）

ISSN： 0098-8472

年卷期： 2020 年 177 卷

页码：

收录情况： SCI

摘要： 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.

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