title: Potassium uptake supporting plant growth in the absence of AKT1 channel activity: Inhibition by ammonium and stimulation by sodium.
abstract: A transferred-DNA insertion mutant of Arabidopsis that lacks AKT1 inward-rectifying K+ channel activity in root cells was obtained previously by a reverse-genetic strategy, enabling a dissection of the K+-uptake apparatus of the root into AKT1 and non-AKT1 components. Membrane potential measurements in root cells demonstrated that the AKT1 component of the wild-type K+ permeability was between 55 and 63% when external [K+] was between 10 and 1,000 microM, and NH4+ was absent. NH4+ specifically inhibited the non-AKT1 component, apparently by competing for K+ binding sites on the transporter(s). This inhibition by NH4+ had significant consequences for akt1 plants: K+ permeability, 86Rb+ fluxes into roots, seed germination, and seedling growth rate of the mutant were each similarly inhibited by NH4+. Wild-type plants were much more resistant to NH4+. Thus, AKT1 channels conduct the K+ influx necessary for the growth of Arabidopsis embryos and seedlings in conditions that block the non-AKT1 mechanism. In contrast to the effects of NH4+, Na+ and H+ significantly stimulated the non-AKT1 portion of the K+ permeability. Stimulation of akt1 growth rate by Na+, a predicted consequence of the previous result, was observed when external [K+] was 10 microM. Collectively, these results indicate that the AKT1 channel is an important component of the K+ uptake apparatus supporting growth, even in the "high-affinity" range of K+ concentrations. In the absence of AKT1 channel activity, an NH4+-sensitive, Na+/H+-stimulated mechanism can suffice.
authors.affiliation: Department of Botany, University of Wisconsin, Madison, Wisconsin 53706, USA.
authors.forename: E P
authors.initials: EP
authors.lastname: Spalding
authors.forename: R E
authors.initials: RE
authors.lastname: Hirsch
authors.forename: D R
authors.initials: DR
authors.lastname: Lewis
authors.forename: Z
authors.initials: Z
authors.lastname: Qi
authors.forename: M R
authors.initials: MR
authors.lastname: Sussman
authors.forename: B D
authors.initials: BD
authors.lastname: Lewis
mesh_terms: D017360:Arabidopsis; D029681:Arabidopsis Proteins; D001692:Biological Transport / Q000187:drug effects / Q000502:physiology; D018506:Gene Expression Regulation, Plant / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D016254:Mutagenesis, Insertional / Q000502:physiology; D010940:Plant Proteins / Q000235:genetics / Q000378:metabolism*; D018517:Plant Roots / Q000737:chemistry* / Q000166:cytology / Q000254:growth & development; D011188:Potassium / Q000493:pharmacokinetics*; D015221:Potassium Channels / Q000235:genetics / Q000378:metabolism*; D000644:Quaternary Ammonium Compounds / Q000493:pharmacokinetics*; D012413:Rubidium / Q000493:pharmacokinetics; D012964:Sodium / Q000493:pharmacokinetics*
chemical_list: D029681:Arabidopsis Proteins; D010940:Plant Proteins; D015221:Potassium Channels; D000644:Quaternary Ammonium Compounds; C074500:AKT1 protein, Arabidopsis; D012964:Sodium; D012413:Rubidium; D011188:Potassium