Protection of Plasma Membrane K+ Transport by the Salt Overly Sensitive1 Na+-H+ Antiporter during Salinity Stress

Abstract

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 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.