PMID:21134373

Citation	Boogerd, FC, Ma, H, Bruggeman, FJ, van Heeswijk, WC, García-Contreras, R, Molenaar, D, Krab, K and Westerhoff, HV (2011) 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. FEBS Lett. 585:23-8
Abstract	The 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 NH(4)(+) concentrations to sustain growth. Revisiting experimental evidence, we find the permeability assays reporting passive NH(3) import inconclusive. As an inevitable consequence of the proposed NH(4)(+) transport, outward permeation of NH(3) 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.
Links	PubMed Online version:10.1016/j.febslet.2010.11.055
Keywords	Ammonia/metabolism; Cation Transport Proteins/physiology; Escherichia coli/metabolism; Escherichia coli Proteins/physiology; Hydrogen-Ion Concentration; Models, Biological; Nucleotidyltransferases/physiology; PII Nitrogen Regulatory Proteins/physiology; Prokaryotic Cells/metabolism; Quaternary Ammonium Compounds/metabolism; Substrate Cycling/physiology
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Significance

Gene product	Qualifier	GO Term	Evidence Code	with/from	Aspect	Extension	Notes	Status
ECOLI:GLNK		GO:0015696: ammonium transport	ECO:0000315:		P		Figure 2. shows how glnK binds with AmtB to physically block the exit of ammonia from the cytoplasm.	complete

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