Olías Raquel, Eljakaoui Zakia, Li Jun, De Morales Paz Alvarez, Marín-Manzano Mari Carmen, Pardo Jose M, Belver Andrés
Estación Experimental del Zaidín, Consejo Superior de Investigaciones Científicas, Granada, Spain.
Plant Cell Environ. 2009 Jul;32(7):904-16. doi: 10.1111/j.1365-3040.2009.01971.x. Epub 2009 Mar 3.
We have identified a plasma membrane Na(+)/H(+) antiporter gene from tomato (Solanum lycopersicum), SlSOS1, and used heterologous expression in yeast to confirm that SlSOS1 was the functional homolog of AtSOS1. Using post-transcriptional gene silencing, we evaluated the role played by SlSOS1 in long-distance Na(+) transport and salt tolerance of tomato. Tomato was used because of its anatomical structure, more complex than that of Arabidopsis, and its agricultural significance. Transgenic tomato plants with reduced expression of SlSOS1 exhibited reduced growth rate compared to wild-type (WT) plants in saline conditions. This sensitivity correlated with higher accumulation of Na(+) in leaves and roots, but lower contents in stems of silenced plants under salt stress. Differential distribution of Na(+) and lower net Na(+) flux were observed in the xylem sap in the suppressed plants. In addition, K(+) concentration was lower in roots of silenced plants than in WT. Our results demonstrate that SlSOS1 antiporter is not only essential in maintaining ion homeostasis under salinity, but also critical for the partitioning of Na(+) between plant organs. The ability of tomato plants to retain Na(+) in the stems, thus preventing Na(+) from reaching the photosynthetic tissues, is largely dependent on the function of SlSOS1.
我们从番茄(Solanum lycopersicum)中鉴定出一个质膜Na(+)/H(+)逆向转运蛋白基因SlSOS1,并通过在酵母中的异源表达证实SlSOS1是拟南芥AtSOS1的功能同源物。利用转录后基因沉默技术,我们评估了SlSOS1在番茄长距离Na(+)转运和耐盐性中所起的作用。选用番茄是因为其解剖结构比拟南芥更复杂,且具有农业重要性。与野生型(WT)植株相比,SlSOS1表达降低的转基因番茄植株在盐胁迫条件下生长速率降低。这种敏感性与盐胁迫下沉默植株叶片和根中Na(+)的较高积累相关,但茎中的含量较低。在受抑制植株的木质部汁液中观察到Na(+)的差异分布和较低的净Na(+)通量。此外,沉默植株根中的K(+)浓度低于WT植株。我们的结果表明,SlSOS1逆向转运蛋白不仅在盐胁迫下维持离子稳态中至关重要,而且对Na(+)在植物器官间的分配也至关重要。番茄植株将Na(+)保留在茎中从而防止Na(+)到达光合组织的能力很大程度上依赖于SlSOS1的功能。