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 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.
Qi
Zhi
Z
Department of Botany, University of Wisconsin, Madison, WI 53706, USA.
Spalding
Edgar P
EP
D017360:Arabidopsis / Q000187:drug effects / Q000235:genetics / Q000254:growth & development / Q000378:metabolism*; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D002463:Cell Membrane Permeability / Q000187:drug effects; D003593:Cytoplasm / Q000378:metabolism; D017343:Genes, Plant; D006706:Homeostasis; D017136:Ion Transport; D009154:Mutation; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000235:genetics / Q000378:metabolism; D036226:Seedlings / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism; D012964:Sodium / Q000378:metabolism / Q000494:pharmacology; D012965:Sodium Chloride / Q000494:pharmacology; D017923:Sodium-Hydrogen Exchangers / Q000235:genetics / Q000378:metabolism*
D029681:Arabidopsis Proteins; D015221:Potassium Channels; C477653:SOS1 protein, Arabidopsis; D017923:Sodium-Hydrogen Exchangers; C074500:AKT1 protein, Arabidopsis; D012965:Sodium Chloride; D012964:Sodium; D011188:Potassium