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AmtB‐mediated NH 3 transport in prokaryotes must be active and as a consequence regulation of transport by GlnK is mandatory to limit futile cycling of NH 4 + / NH 3
Author(s) -
Boogerd Fred C.,
Ma Hongwu,
Bruggeman Frank J.,
van Heeswijk Wally C.,
García-Contreras Rodolfo,
Molenaar Douwe,
Krab Klaas,
Westerhoff Hans V.
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.11.055
Subject(s) - intracellular , ammonium , biophysics , cycling , chemistry , microbiology and biotechnology , permeability (electromagnetism) , transport protein , biochemistry , limit (mathematics) , biology , membrane , organic chemistry , history , mathematical analysis , mathematics , archaeology
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 intracellularNH 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 proposedNH 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.