Abstract
The role of the K+ transport systems encoded by the kefB (formerly trkB) and kefC (formerly trkC) genes of Escherichia coli in K+ efflux has been investigated. The rate of efflux produced by N-ethylmaleimide (NEM), increased turgor pressure, alkalinization of the cytoplasm, or 2,4-dinitrophenol in a mutant with null mutations in both kef genes was compared with the rate of efflux in a wild-type strain for kef. The results show that these two genes encode the major paths for NEM-stimulated efflux. However, neither efflux system appears to be a significant path of K+ efflux produced by high turgor pressure, by alkalinization of the cytoplasm, or by addition of high concentrations of 2,4-dinitrophenol. Therefore, this species must have at least one other system, besides those encoded by kefB and kefC, capable of mediating a high rate of K+ efflux. The high, spontaneous rate of K+ efflux characteristic of the kefC121 mutation increases further when the strain is treated with NEM. Therefore, the mutational defect that leads to spontaneous efflux in this strain does not abolish the site(s) responsible for the action of NEM.
MeSH Terms
2,4-Dinitrophenol
Betaine/pharmacology
Biological Transport/drug effects
Carrier Proteins/metabolism
Dinitrophenols/pharmacology
Escherichia coli/genetics,metabolism
Ethanolamines/pharmacology
Ethylmaleimide/pharmacology
Genes, Bacterial
Mutation
Potassium/metabolism
Potassium-Hydrogen Antiporters
Chemicals
Carrier Proteins
Dinitrophenols
Ethanolamines
Potassium-Hydrogen Antiporters
Betaine
diethanolamine
Ethylmaleimide
2,4-Dinitrophenol
Potassium
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Bakker E P
Booth I R
Dinnbier U
Epstein W
Gajewska A
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