Fig. 7. Model for regulation of the interaction between GlnK and AmtB. In conditions of nitrogen limitation (–N), GlnK is predominantly in its fully uridylylated state and is not strongly membrane associated (non-shaded GlnK indicates the minority species in each situation). AmtB is active and will effectively scavenge ammonium from the surrounding medium. When the cellular nitrogen status changes, e.g. as a consequence of a sudden rise in the availability of extracellular ammonium, GlnK is deuridylylated rapidly and the unmodified form of the protein associates tightly with AmtB in the inner membrane. This association reduces the activity of AmtB and ammonium is no longer transported actively into the cell. This process is rapidly reversible, but in the event that the nitrogen status remains high, transcription of the glnK–amtB operon will cease due to dephosphorylation of the activator protein NtrC.