Saier M H, Straud H, Massman L S, Judice J J, Newman M J, Feucht B U
J Bacteriol. 1978 Mar;133(3):1358-67. doi: 10.1128/jb.133.3.1358-1367.1978.
Several carbohydrate permease systems in Salmonella typhimurium and Escherichia coli are sensitive to regulation by the phosphoenolpyruvate:sugar phosphotransferase system. Mutant Salmonella strains were isolated in which individual transport systems had been rendered insensitive to regulation by sugar substrates of the phosphotransferase system. In one such strain, glycerol uptake was insensitive to regulation; in another, the maltose transport system was resistant to inhibition; and in a third, the regulatory mutation specifically rendered the melibiose permease insensitive to regulation. An analogous mutation in E. coli abolished inhibition of the transport of beta-galactosides via the lactose permease system. The mutations were mapped near the genes which code for the affected transport proteins. The regulatory mutations rendered utilization of the particular carbohydrates resistant to inhibition and synthesis of the corresponding catabolic enzymes partially insensitive to repressive control by sugar substrates of the phosphotransferase system. Studies of repression of beta-galactosidase synthesis in E. coli were conducted with both lactose and isopropyl beta-thiogalactoside as exogenous sources of inducer. Employing high concentrations of isopropyl beta-thiogalactoside, repression of beta-galactosidase synthesis was not altered by the lactose-specific transport regulation-resistant mutation. By contrast, the more severe repression observed with lactose as the exogenous source of inducer was partially abolished by this regulatory mutation. The results support the conclusions that several transport systems, including the lactose permease system, are subject to allosteric regulation and that inhibition of inducer uptake is a primary cause of the repression of catabolic enzyme synthesis.
糖磷酸转移酶系统的调节敏感。分离出了突变的沙门氏菌菌株，其中各个转运系统对磷酸转移酶系统的糖底物调节变得不敏感。在一种这样的菌株中，甘油摄取对调节不敏感；在另一种菌株中，麦芽糖转运系统对抑制有抗性；在第三种菌株中，调节突变使蜜二糖通透酶对调节特别不敏感。大肠杆菌中的类似突变消除了通过乳糖通透酶系统对β-半乳糖苷转运的抑制。这些突变被定位在编码受影响转运蛋白的基因附近。调节突变使特定碳水化合物的利用对抑制有抗性，并且相应分解代谢酶的合成对磷酸转移酶系统的糖底物的阻遏控制部分不敏感。以乳糖和异丙基β-硫代半乳糖苷作为诱导剂的外源来源，对大肠杆菌中β-半乳糖苷酶合成的阻遏进行了研究。使用高浓度的异丙基β-硫代半乳糖苷时，β-半乳糖苷酶合成的阻遏不会因乳糖特异性转运调节抗性突变而改变。相比之下，以乳糖作为诱导剂的外源来源时观察到的更严重的阻遏被这种调节突变部分消除。结果支持以下结论：包括乳糖通透酶系统在内的几种转运系统受到变构调节，并且诱导剂摄取的抑制是分解代谢酶合成阻遏的主要原因。
