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-re ctifying K+ channel activity in root cells was obtained previously by a rev erse-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+ per meability was between 55 and 63% when external [K+] was between 10 and 1,00 0 mu M, and NH4+ was absent. NH4+ specifically inhibited the non-AKT1 compo nent, apparently by competing for K+ binding sites on the transporter(s). T his inhibition by NH+4 had significant consequences for akt1 plants: K+ per meability, Rb-86(+) fluxes into roots, seed germination, and seedling growt h rate of the mutant were each similarly inhibited by NH4+. Wild-type plant s were much more resistant to NH4+. Thus, AKT1 channels conduct the K+ infl ux necessary for the growth of Arabidopsis embryos and seedlings in conditi ons 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+ permeabi lity. Stimulation of akt1 growth rate by Na+, a predicted consequence of th e previous result, was observed when external [K+] was 10 mu M. Collectivel y, these results indicate that the AKT1 channel is an important component o f the K+ uptake apparatus supporting growth, even in the "high-affinity" ra nge of K+ concentrations. In the absence of AKT1 channel activity an NH4+-s ensitive, Na+/H+-stimulated mechanism can suffice.