Fields K L, Luria S E
J Bacteriol. 1969 Jan;97(1):57-63. doi: 10.1128/jb.97.1.57-63.1969.
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.
研究了大肠杆菌素E1和K对大肠杆菌主动转运β-D-半乳糖苷和α-甲基-D-葡萄糖苷（αMG）的影响。这些大肠杆菌素强烈抑制细菌对硫代甲基半乳糖苷（TMG）的积累，并导致先前积累的TMG快速排出。抑制作用仅限于半乳糖苷转运的积累阶段；邻硝基苯半乳糖苷的水解速率仅略有影响，其水解速率取决于乳糖通透酶系统对底物的转运。在导致TMG积累完全被抑制的条件下，αMG的积累对这些大肠杆菌素的抑制具有高度抗性。大肠杆菌素对转运的这些影响在质量上类似于叠氮化钠的影响。通过假设大肠杆菌素E1和K抑制TMG积累中能量依赖的步骤，但不影响由特定转运机制介导的半乳糖苷的易化扩散来解释这些发现。αMG的持续积累归因于这样一个事实，即该化合物被大肠杆菌细胞通过磷酸烯醇丙酮酸依赖的转运系统作为磷酸化化合物储存，而不是通过三磷酸腺苷连接的积累机制。
