The effect of colicins E1 and K on active transport of beta-d-galactosides and of alpha-methyl-d-glucoside (alphaMG) by Escherichia coli was studied. These colicins strongly inhibited the accumulation of thio-methyl-galactoside (TMG) by bacteria and caused rapid exit of previously accumulated TMG. The inhibition effect was limited to the accumulation phase of galactoside transport; the rate of hydrolysis of o-nitrophenyl galactoside, which is dependent on transport of the substrate by the lactose-permease system, was only slightly affected. The accumulation of alphaMG was highly resistant to inhibition by these colicins under conditions which caused complete suppression of TMG accumulation. These effects of the colicins on transport resemble qualitatively those of sodium azide. The findings were interpreted by assuming that colicins E1 and K inhibit the energy-dependent steps in the accumulation of TMG but do not affect facilitated diffusion of galactosides mediated by the specific transport mechanism. The continued accumulation of alphaMG was attributed to the fact that this compound is stored by E. coli cells as a phosphorylated compound by a phosphoenolpyruvate-dependent transport system rather than by an adenosine triphosphate-linked accumulation mechanism.
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