Abstract
The accumulation of 204T1+ by Escherichia coli occurs primarily via either of two K+ transport systems called Kdp and TrkA. T1+ influx is inhibited and T1+ efflux is stimulated by the addition of K+ to the assay medium. Mutants defective in both the Kdp and TrkA systems accumulate little T1+. Uptake of triphenylmethylphosphonium, a lipid-soluble cation whose distribution is widely used to estimate the membrane electrical potential in bacteria, occurs to about the same extent in mutants that accumulate little T1+ as in strains that accumulate T1+ to high levels. These findings indicate that T1+ may be useful as a probe of bacterial K+ transport systems but is not a reliable indicator of the membrane electrical potential in E. coli.
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