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Protection of Plasma Membrane K⁺ Transport by the Salt Overly Sensitive1 Na⁺-H⁺ Antiporter during Salinity Stress¹

Department of Botany, University of Wisconsin, Madison, Wisconsin 53706

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.

Article, publication date, and citation information can be found at www.plantphysiol.org/cgi/doi/10.1104/pp.104.049213.

^* Corresponding author; e-mail spalding{at}wisc.edu; fax 608–262–7509.

Received July 6, 2004; returned for revision August 3, 2004; accepted August 4, 2004.

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