The molecular basis of K+ exclusion by the Escherichia coli ammonium channel AmtB

J Biol Chem. 2013 May 17;288(20):14080-14086. doi: 10.1074/jbc.M113.457952. Epub 2013 Apr 1.

Abstract

Members of the Amt family of channels mediate the transport of ammonium. The form of ammonium, NH3 or NH4(+), carried by these proteins remains controversial, and the mechanism by which they select against K(+) ions is unclear. We describe here a set of Escherichia coli AmtB proteins carrying mutations at the conserved twin-histidine site within the conduction pore that have altered substrate specificity and now transport K(+). Subsequent work established that AmtB-mediated K(+) uptake occurred against a concentration gradient and was membrane potential-dependent. These findings indicate that the twin-histidine element serves as a filter to prevent K(+) conduction and strongly support the notion that Amt proteins transport cations (NH4(+) or, in mutant proteins, K(+)) rather than NH3 gas molecules through their conduction pores.

Keywords: Ammonium Transport; Amt Proteins; Escherichia coli; Ion Channels; Membrane Transport; Microbiology; Potassium Transport.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Biological Transport
  • Cation Transport Proteins / metabolism*
  • Cytoplasm / metabolism
  • Dose-Response Relationship, Drug
  • Escherichia coli / metabolism*
  • Escherichia coli Proteins / metabolism*
  • Hydrogen-Ion Concentration
  • Ions
  • Membrane Potentials
  • Mutation
  • Potassium / metabolism*
  • Protein Conformation
  • Quaternary Ammonium Compounds / metabolism
  • Substrate Specificity

Substances

  • AmtB protein, E coli
  • Cation Transport Proteins
  • Escherichia coli Proteins
  • Ions
  • Quaternary Ammonium Compounds
  • Potassium