Overexpression of SlSOS2 (SlCIPK24) confers salt tolerance to transgenic tomato.

The Ca(2+)-dependent SOS pathway has emerged as a key mechanism in the homeostasis of Na(+) and K(+) under saline conditions. We have identified and functionally characterized the gene encoding the calcineurin-interacting protein kinase of the SOS pathway in tomato, SlSOS2. On the basis of protein sequence similarity and complementation studies in yeast and Arabidopsis, it can be concluded that SlSOS2 is the functional tomato homolog of Arabidopsis AtSOS2 and that SlSOS2 operates in a tomato SOS signal transduction pathway. The biotechnological potential of SlSOS2 to provide salt tolerance was evaluated by gene overexpression in tomato (Solanum lycopersicum L. cv. MicroTom). The better salt tolerance of transgenic plants relative to non-transformed tomato was shown by their faster relative growth rate, earlier flowering and higher fruit production when grown with NaCl. The increased salinity tolerance of SlSOS2-overexpressing plants was associated with higher sodium content in stems and leaves and with the induction and up-regulation of the plasma membrane Na(+)/H(+) (SlSOS1) and endosomal-vacuolar K(+), Na(+)/H(+) (LeNHX2 and LeNHX4) antiporters, responsible for Na(+) extrusion out of the root, active loading of Na(+) into the xylem, and Na(+) and K(+) compartmentalization.

The Na(+)/H(+) exchanger SOS1 controls extrusion and distribution of Na(+) in tomato plants under salinity conditions.

Maintaining a high K(+)/Na(+) ratio in the cell cytosol, along with the transport processes implicated in the xylem and phloem loading/unloading of Na(+) in plants (long-distance transport) are key aspects in plant salt tolerance. The Ca(2+)-dependent SOS pathway regulating Na(+) and K(+) homeostasis and long-distance Na(+) transport has been reported in Arabidopsis. However, Arabidopsis might not be the best model to analyze the involvement of the SOS pathway in long-distance Na(+) transport due to the very short stem of these plants which do not allow a precise dissection of the relative content of Na(+) in stem versus leaf. This separation would be critical to assess the role of SOS1 in xylem loading/unloading, Na(+) export by roots, retention in stems and the differential distribution/accumulation in old leaves. Towards this goal, tomato might represent a superior model due to its anatomical structure and agricultural significance. We recently demonstrated the key role played by the plasma membrane Na(+)/H(+) antiporter SlSOS1 in salt tolerance in tomato by maintaining ion homeostasis under salinity stress and in the partitioning of Na(+) in plant organs.

The plasma membrane Na+/H+ antiporter SOS1 is essential for salt tolerance in tomato and affects the partitioning of Na+ between plant organs.

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.