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鼠伤寒沙门氏菌中碳水化合物转运活性的调控:利用磷酸甘油转运系统为溶质摄取提供能量

Regulation of carbohydrate transport activities in Salmonella typhimurium: use of the phosphoglycerate transport system to energize solute uptake.

作者信息

Saier M H, Feucht B U

出版信息

J Bacteriol. 1980 Feb;141(2):611-7. doi: 10.1128/jb.141.2.611-617.1980.

Abstract

The phosphoglycerate transport system was employed to supply energy-depleted, lysozyme-treated Salmonella typhimurium cells with a continuous intracellular source of phosphoenolpyruvate. When the cells had been induced to high levels of the phosphoglycerate transport system, a low extracellular concentration of phosphoenolpyruvate (0.1 mM) half maximally stimulated uptake of methyl alpha-glucoside via the phosphoenolpyruvate:sugar phosphotransferase system. If the phosphoglycerate transport system was not induced before energy depletion, 100 times this concentration of phosphoenolpyruvate was required for half-maximal stimulation. Phosphoenolpyruvate could not be replaced by other energy sources if potassium fluoride (an inhibitor of enolase) was present. Inhibition of [14C]-glycerol uptake into energy-depleted cells by methyl alpha-glucoside was demonstrated. A concentration of phosphoenolpyruvate which stimulated methyl alpha-glucoside accumulation counteracted the inhibitory effect of the glucoside. In the presence of potassium fluoride, phosphoenolpyruvate could not be replaced by other energy sources. Inhibition of glycerol uptake by methyl alpha-glucoside in intact untreated cells was also counteracted by phosphoenolpyruvate, but several energy sources were equally effective; potassium fluoride was without effect. These and other results were interpreted in terms of a mechanism in which the relative proportions of the phosphorylated and nonphosphorylated forms of a cell constituent influence the activity of the glycerol transport system.

摘要

磷酸甘油酸转运系统被用于为能量耗尽且经溶菌酶处理的鼠伤寒沙门氏菌细胞提供细胞内持续的磷酸烯醇丙酮酸来源。当细胞被诱导至高水平的磷酸甘油酸转运系统时,细胞外低浓度的磷酸烯醇丙酮酸(0.1 mM)可通过磷酸烯醇丙酮酸:糖磷酸转移酶系统半最大程度地刺激α-甲基葡萄糖苷的摄取。如果在能量耗尽前未诱导磷酸甘油酸转运系统,则需要该浓度100倍的磷酸烯醇丙酮酸才能达到半最大刺激。如果存在氟化钾(烯醇酶抑制剂),则磷酸烯醇丙酮酸不能被其他能量来源替代。已证明α-甲基葡萄糖苷可抑制能量耗尽细胞对[14C]甘油的摄取。刺激α-甲基葡萄糖苷积累的磷酸烯醇丙酮酸浓度可抵消该糖苷的抑制作用。在存在氟化钾的情况下,磷酸烯醇丙酮酸不能被其他能量来源替代。在完整未处理的细胞中,α-甲基葡萄糖苷对甘油摄取的抑制作用也可被磷酸烯醇丙酮酸抵消,但几种能量来源同样有效;氟化钾无作用。这些及其他结果是根据一种机制来解释的,即细胞成分的磷酸化和非磷酸化形式的相对比例会影响甘油转运系统的活性。

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