Abstract

Colicin K causes a rapid and drastic reduction of the membrane potential of Escherichia coli cells, as measured by the uptake of the lipophilic cation triphenylmethylphosphonium. The colicin causes no major changes in the pH gradient, as measured by the uptake of butyric acid. The decrease in membrane potential following addition of colicin K to the cells is a prompt response that parallels or precedes known physiological effects such as efflux of accumulated substrates. Hence the loss of membrane potential qualifies as the primary action by which the colicin uncouples membrane-associated function from respiration. Certain peculiarities of bacterial cells pretreated with EDTA in their response to uncoupling agents and lipophilic ions are described.

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