Barnes E M, Kaback H R
Proc Natl Acad Sci U S A. 1970 Aug;66(4):1190-8. doi: 10.1073/pnas.66.4.1190.
The transport of beta-galactosides by isolated membrane preparations from Escherichia coli strains containing a functional y gene is markedly stimulated by the conversion of D-lactate to pyruvate. The addition of D-lactate to these membrane preparations produces a 19-fold increase in the initial rate of uptake and a 10-fold stimulation of the steady-state level of intramembranal lactose or thiomethylgalactoside. Succinate, DL-alpha-hydroxybutyrate, and L-lactate partially replace D-lactate, but are much less effective; ATP and P-enolpyruvate, in addition to a number of other metabolites and cofactors, do not stimulate lactose transport by the vesicles. Lactose uptake by the membrane preparations in the presence of D-lactate requires oxygen, and is blocked by electron transport inhibitors and proton conductors; however, uptake is not significantly inhibited by high concentrations of arsenate or oligomycin. Furthermore, the P-enolpyruvate-P-transferase system is not involved in beta-galactoside transport by the E. coli membrane vesicles. The findings indicate that the beta-galactoside uptake system is coupled to the membrane-bound D-lactic dehydrogenase via an electron transport chain but does not involve oxidative phosphorylation.
来自含有功能性y基因的大肠杆菌菌株的分离膜制剂对β-半乳糖苷的转运,会因D-乳酸转化为丙酮酸而受到显著刺激。向这些膜制剂中添加D-乳酸会使初始摄取速率增加19倍,并使膜内乳糖或硫代甲基半乳糖苷的稳态水平提高10倍。琥珀酸、DL-α-羟基丁酸和L-乳酸可部分替代D-乳酸,但效果要差得多;ATP和磷酸烯醇丙酮酸,以及许多其他代谢物和辅因子,均不会刺激囊泡对乳糖的转运。在D-乳酸存在下,膜制剂对乳糖的摄取需要氧气,并会被电子传递抑制剂和质子导体阻断;然而,高浓度的砷酸盐或寡霉素对摄取没有显著抑制作用。此外,磷酸烯醇丙酮酸-磷酸转移酶系统不参与大肠杆菌膜囊泡对β-半乳糖苷的转运。这些发现表明,β-半乳糖苷摄取系统通过电子传递链与膜结合的D-乳酸脱氢酶偶联,但不涉及氧化磷酸化。