Ye J J, Saier M H
Department of Biology, University of California at San Diego, La Jolla 92093-0116, USA.
J Bacteriol. 1996 Jun;178(12):3557-63. doi: 10.1128/jb.178.12.3557-3563.1996.
By using both metabolizable and nonmetabolizable sugar substrates of the phosphoenolpyruvate-dependent phosphotransferase system (PTS), we show that PTS sugar uptake into intact cells and membrane vesicles of Lactococcus lactis and Bacillus subtilis is strongly inhibited by high concentrations of any of several metabolizable PTS sugars. Inhibition requires phosphorylation of seryl residue 46 in the phosphocarrier protein of the PTS, HPr, by the metabolite-activated, ATP-dependent protein kinase. Inhibition does not occur when wild-type HPr is replaced by the S46A mutant form of this protein either in vesicles of L. lactis or B. subtilis or in intact cells of B. subtilis. Nonmetabolizable PTS sugar analogs such as 2-deoxyglucose inhibit PTS sugar uptake by a distinct mechanism that is independent of HPr(ser-P) and probably involves cellular phosphoenolpyruvate depletion.
通过使用磷酸烯醇丙酮酸依赖性磷酸转移酶系统(PTS)的可代谢和不可代谢糖底物,我们发现,高浓度的几种可代谢PTS糖中的任何一种都会强烈抑制乳酸乳球菌和枯草芽孢杆菌完整细胞及膜囊泡对PTS糖的摄取。这种抑制作用需要代谢物激活的、依赖ATP的蛋白激酶将PTS的磷酸载体蛋白HPr中的丝氨酸残基46磷酸化。当野生型HPr被该蛋白的S46A突变形式取代时,无论是在乳酸乳球菌或枯草芽孢杆菌的膜囊泡中,还是在枯草芽孢杆菌的完整细胞中,都不会发生抑制作用。不可代谢的PTS糖类似物,如2-脱氧葡萄糖,通过一种独立于HPr(丝氨酸-P)的独特机制抑制PTS糖的摄取,这可能涉及细胞内磷酸烯醇丙酮酸的消耗。