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 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 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 NH₄⁺-sensitive, Na⁺/H⁺-stimulated mechanism can suffice.