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This review article summarises the role of membrane transporters and their regulatory kinases in minimising the toxicity of Na+ in the plant under salt stress. The salt-tolerant plants keep their cytosolic level of Na+ up to 10–50mM. The first line of action in this context is the generation of proton motive force by the plasma membrane H+-ATPase. The generated proton motive force repolarises the membrane that gets depolarised due to passive uptake of Na+ under salt stress. The proton motive force generated also drives the plasma membrane Na+/H+ antiporter, SOS1 that effluxes the cytosolic Na+ back into the environment. At the intracellular level, Na+ is sequestered by the vacuole. Vacuolar Na+ uptake is mediated by Na+/H+ antiporter, NHX, driven by the electrochemical gradient for H+, generated by tonoplast H+ pumps, both H+ATPase and PPase. However, it is the expression of the regulatory kinases that make these transporters active through post-translational modification enabling them to effectively manage the cytosolic level of Na+, which is essential for tolerance to salinity in plants. Yet our knowledge of the expression and functioning of the regulatory kinases in plant species differing in tolerance to salinity is scant. Bioinformatics-based identification of the kinases like OsCIPK24 in crop plants, which are mostly salt-sensitive, may enable biotechnological intervention in making the crop cultivar more salt-tolerant, and effectively increasing its annual yield.

Post-translational regulation of the membrane transporters contributing to salt tolerance in plants