Protection of plasma membrane K+ transport by the salt overly sensitive1 Na+-H+ antiporter during salinity stress

Physicochemical similarities between K+ and Na+ result in interactions between their homeostatic mechanisms. The physiological interactions between these two ions was investigated by examining aspects of K+ nutrition in the Arabidopsis salt overly sensitive (sos) mutants, and salt sensitivity in the K+ transport mutants akt1 (Arabidopsis K+ transporter) and skor (shaker-like K+ outward-rectifying channel). The K+-uptake ability (membrane permeability) of the sos mutant root cells measured electrophysiologically was normal in control conditions. Also, growth rates of these mutants in Na+-free media displayed wild-type K+ dependence. However, mild salt stress (50 mM NaCl) strongly inhibited root-cell K+ permeability and growth rate in K+-limiting conditions of sos1 but not wild-type plants. Increasing K+ availability partially partially rescued the sos1 growth phenotype. Therefore, it appears that in the presence of Na+, the SOS1 Na+-H+ antiporter is necessary for protecting the K+ permeability on which growth depends. The hypothesis that the elevated cytoplasmic Na+ levels predicted to result from loss of SOS1 function impaired the K+ permeability was tested by introducing 10 mm NaCl into the cytoplasm of a patch-clamped wild-type root cell. Complete loss of AKT1 K+ channel activity ensued. AKT1 is apparently a target of salt stress in sos1 plants, resulting in poor growth due to impaired K+ uptake. Complementary studies showed that akt1 seedlings were salt sensitive during early seedling development, but skor seedlings were normal. Thus, the effect of Na+ on K+ transport is probably more important at the uptake stage than at the xylem loading stage.