AmtB-mediated NH3 transport in prokaryotes must be active and as a consequence regulation of transport by GlnK is mandatory to limit futile cycling of NH4+/NH3

AbstractThe nature of the ammonium import into prokaryotes has been controversial. A systems biological approach makes us hypothesize that AmtB-mediated import must be active for intracellular NH4+ concentrations to sustain growth. Revisiting experimental evidence, we find the permeability assays reporting passive NH3 import inconclusive. As an inevitable consequence of the proposed NH4+ transport, outward permeation of NH3 constitutes a futile cycle. We hypothesize that the regulatory protein GlnK is required to fine-tune the active transport of ammonium in order to limit futile cycling whilst enabling an intracellular ammonium level sufficient for the cell’s nitrogen requirements