Saier M H, Schmidt M R
J Bacteriol. 1981 Jan;145(1):391-7. doi: 10.1128/jb.145.1.391-397.1981.
Vectorial transphosphorylation of hexitols, catalyzed by enzymes II of the bacterial phosphotransferase system, was studied in intact cells and membrane vesicles of Escherichia coli. In strains depleted of phosphoenolpyruvate and unable to metabolize the internal hexitol phosphate, internal mannitol-1-phosphate stimulated uptake of extracellular [14C]mannitol, whereas external mannitol stimulated release of [14C]mannitol from the intracellular [14C]mannitol-1-phosphate pool. The stoichiometry of mannitol uptake to mannitol release was 1:1. Glucitol did not promote release of [14C]mannitol from the mannitol phosphate pool but stimulated release of [14C]glucitol from internal glucitol phosphate pools when the glucitol enzyme II was induced to high levels. In E coli cells and membrane vesicles, both vectorial and nonvectorial transphosphorylation reactions of hexitols and hexoses were demonstrated. The nonvectorial reactions, but not the vectorial reactions, catalyzed by the mannitol and glucose enzymes II, were inhibited by p-chloromercuriphenyl sulfonate, a membrane-impermeable sulfhydryl reagent which inactivates enzymes II. Similarly, glucose-6-sulfate, an inhibitor of the glucose enzyme II-catalyzed transphosphorylation reaction, specifically inhibited the nonvectorial reaction. This compound was shown to be a noncompetitive inhibitor of methyl alpha-glucoside phosphorylation employing phospho-HPr as the phosphate donor. It apparently exerts its inhibitory effect by exclusive binding to the sugar phosphate binding site on the enzyme II complex. The results are consistent with the conclusion that enzymes II can exist in two distinct dispositions in the membrane, one of which catalyzes vectorial transphosphorylation, and the other catalyzes nonvectorial transphosphorylation.
在大肠杆菌的完整细胞和膜囊泡中,研究了由细菌磷酸转移酶系统的酶II催化的己糖醇的向量转磷酸化作用。在缺乏磷酸烯醇丙酮酸且无法代谢细胞内己糖醇磷酸的菌株中,细胞内的1-磷酸甘露醇刺激了细胞外[14C]甘露醇的摄取,而细胞外甘露醇则刺激了[14C]甘露醇从细胞内[14C]1-磷酸甘露醇池中释放出来。甘露醇摄取与甘露醇释放的化学计量比为1:1。当诱导葡糖醇酶II达到高水平时,葡糖醇不会促进[14C]甘露醇从磷酸甘露醇池中释放,但会刺激[14C]葡糖醇从细胞内磷酸葡糖醇池中释放。在大肠杆菌细胞和膜囊泡中,己糖醇和己糖的向量和非向量转磷酸化反应均得到了证实。对氯汞苯磺酸盐(一种膜不可渗透的巯基试剂,可使酶II失活)抑制了由甘露醇和葡萄糖酶II催化的非向量反应,但不抑制向量反应。同样,葡萄糖-6-硫酸盐(葡萄糖酶II催化的转磷酸化反应的抑制剂)特异性地抑制了非向量反应。该化合物被证明是使用磷酸化组氨酸磷酸蛋白作为磷酸供体时α-甲基葡萄糖苷磷酸化的非竞争性抑制剂。它显然通过排他性地结合酶II复合物上的糖磷酸结合位点发挥其抑制作用。结果与酶II可以在膜中以两种不同的构象存在这一结论一致,其中一种构象催化向量转磷酸化,另一种构象催化非向量转磷酸化。