Thompson J, Chassy B M
J Bacteriol. 1983 May;154(2):819-30. doi: 10.1128/jb.154.2.819-830.1983.
Streptococcus lactis K1 has the capacity to grow on many sugars, including sucrose and lactose, in the presence of high levels (greater than 500 mM) of 2-deoxy-D-glucose. Initially, growth of the organism was transiently halted by the addition of comparatively low concentrations (less than 0.5 mM) of the glucose analog to the culture. Inhibition was coincident with (i) rapid accumulation of 2-deoxy-D-glucose 6-phosphate (ca. 120 mM) and preferential utilization of phosphoenolpyruvate via the mannose:phosphotransferase system, (ii) depletion of phosphorylated glycolytic intermediates, and (iii) a 60% reduction in intracellular ATP concentration. During the 5- to 10-min period of bacteriostasis the intracellular concentration of 2-deoxy-D-glucose 6-phosphate rapidly declined, and the concentrations of glycolytic intermediates were restored to near-normal levels. When growth resumed, the cell doubling time (Td) and the steady-state levels of 2-deoxy-D-glucose 6-phosphate maintained by the cells were dependent upon the medium concentration of 2-deoxy-D-glucose. Resistance of S. lactis K1 to the potentially toxic analog was a consequence of negative regulation of the mannose:phosphotransferase system by two independent mechanisms. The first, short-term response occurred immediately after the initial "overshoot" accumulation of 2-deoxy-D-glucose 6-phosphate, and this mechanism reduced the activity (fine control) of the mannose:phosphotransferase system. The second, long-term mechanism resulted in repression of synthesis (coarse control) of enzyme IImannose. The two regulatory mechanisms reduced the rate of 2-deoxy-D-glucose translocation via the mannose:phosphotransferase system and minimized the activity of the phosphoenolpyruvate-dependent futile cycle of the glucose analog (J. Thompson and B. M. Chassy, J. Bacteriol. 151:1454-1465, 1982). Phosphoenolpyruvate was thus conserved for transport of the growth sugar and for generation of ATP required for biosynthetic and work functions of the growing cell.
乳酸链球菌K1能够在许多糖类上生长，包括蔗糖和乳糖，前提是存在高水平（大于500 mM）的2-脱氧-D-葡萄糖。最初，向培养物中添加相对低浓度（小于0.5 mM）的葡萄糖类似物会使该生物体的生长暂时停止。抑制作用与以下情况同时发生：（i）2-脱氧-D-葡萄糖6-磷酸（约120 mM）迅速积累，且通过甘露糖：磷酸转移酶系统优先利用磷酸烯醇丙酮酸；（ii）磷酸化糖酵解中间产物耗竭；（iii）细胞内ATP浓度降低60%。在抑菌的5至10分钟期间，2-脱氧-D-葡萄糖6-磷酸的细胞内浓度迅速下降，糖酵解中间产物的浓度恢复到接近正常水平。当生长恢复时，细胞倍增时间（Td）以及细胞维持的2-脱氧-D-葡萄糖6-磷酸的稳态水平取决于培养基中2-脱氧-D-葡萄糖的浓度。乳酸链球菌K1对这种潜在有毒类似物的抗性是由两种独立机制对甘露糖：磷酸转移酶系统进行负调控的结果。第一种是短期反应，在2-脱氧-D-葡萄糖6-磷酸最初“超调”积累后立即发生，该机制降低了甘露糖：磷酸转移酶系统的活性（精细调控）。第二种是长期机制，导致对酶II甘露糖合成的阻遏（粗略调控）。这两种调控机制降低了2-脱氧-D-葡萄糖通过甘露糖：磷酸转移酶系统的转运速率，并使葡萄糖类似物的磷酸烯醇丙酮酸依赖性无效循环的活性降至最低（J. 汤普森和B. M. 查西，《细菌学杂志》151:1454 - 1465，1982）。因此，磷酸烯醇丙酮酸得以保留，用于生长糖类的转运以及为生长细胞的生物合成和生理功能所需的ATP生成。
