Potassium Uptake Supporting Plant Growth in the Absence of AKT1 Channel Activity : Inhibition by Ammonium and Stimulation by Sodium

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 μM, and NH(4) (+) was absent. NH(4) (+) specifically inhibited the non-AKT1 component, apparently by competing for K(+) binding sites on the transporter(s). This inhibition by NH(4) (+) had significant consequences for akt1 plants: K(+) permeability, (86)Rb(+) fluxes into roots, seed germination, and seedling growth rate of the mutant were each similarly inhibited by NH(4) (+). Wild-type plants were much more resistant to NH(4) (+). 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 NH(4) (+), 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 μM. 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 NH(4) (+)-sensitive, Na(+)/H(+)-stimulated mechanism can suffice.