泌盐盐生植物花花柴适应盐碱环境的有效策略是通过其叶表面特殊的泌盐结构盐腺，将体内过多的Na+排出体外而避免盐害，从而增强了其耐盐性。然而，花花柴叶片盐腺是如何将Na+排出体外的泌盐分子机制仍不清楚。研究表明质膜Na+/H+逆向转运蛋白（SOS1）介导的Na+ 外排可能在泌盐植物叶片盐腺泌盐过程中起重要的作用。鉴于此，本项目拟以花花柴为材料，克隆其KcSOS1，利用qRT-PCR技术对盐胁迫下各组织中KcSOS1的转录丰度进行定量分析，并将KcSOS1导入拟南芥突变体atsos1中恢复其耐盐性，以明确KcSOS1具有Na+外排功能；采用RNA干扰技术沉默KcSOS1的表达，分析RNA干扰转化植株各组织中Na+、K+浓度以及叶片盐腺Na+分泌速率和盐腺密度的变化规律，以解析KcSOS1在盐胁迫下介导的Na+外排在花花柴叶片盐腺泌盐中作用机制，这将为盐荒地植被恢复和重建提供重要的科学理论依据。

One of the effective strategies for adaptation of recretohalophyte Karelinia caspica to saline environments is that exclude excess Na+ out of plants via the specialized salt-secreting structure (salt gland) in leaf to avoid salt injury, thus enhancing its salt tolerance. However, the salt-secreting molecular mechanism of leaf salt gland is how to exclude Na+ from K. caspica remain unclear. It has been demonstrated that plasma membrane Na+/H+ antiporter (SOS1) mediated Na+ efflux might play important role in secreting salt of salt gland in recretohalophyte. In view of this, we cloned KcSOS1 from K. caspica; the transcript abundances of KcSOS1 in different tissues were quantificationally analyzed by qRT-PCR technique under salt stress, and overexpression of KcSOS1 into atsos1 of Arabidopsis mutant would rescue its salt tolerance, which confirmed the KcSOS1 had the function of Na+ efflux; the changes of K+, Na+ concentrations in different tissues, Na+ secretion rate- and density in salt gland was investigated after gene silencing of KcSOS1 using RNA interference technique, which elucidated the role of KcSOS1-mediated Na+ efflux in secreting salt of salt gland in K. caspica. This would provide the scientific theory evidence for restoration and reconstruction of ecological vegetation in salt wastelands.