Dills S S, Schmidt M R, Saier M H
J Cell Biochem. 1982;18(2):239-44. doi: 10.1002/jcb.1982.240180211.
Regulation of lactose uptake by the phosphoenolpyruvate-sugar phosphotransferase system (PTS) has been demonstrated in membrane vesicles of Escherichia coli strain ML 308-225. Substrates of the phosphotransferase system inhibited D-lactate energized uptake of lactose but did not inhibit uptake of either L-alanine or L-proline. This inhibition was reversed by intravesicular (but not extravesicular) phosphoenolpyruvate. Lactose uptake was also inhibited by enzyme IIIglc preparations that were shocked into the vesicles, and this inhibition was reversed by phosphoenolpyruvate. Intravesicular HPr and enzyme I stimulated methyl alpha-glycoside uptake but did not inhibit or stimulate lactose accumulation. Vesicles maintained at 0 degree C for several days partially lost 1) the ability to take up lactose, 2) the ability to accumulate PTS substrates, and 3) PTS-mediated regulation. Phosphoenolpyruvate addition restored all of these activities. These results support a mechanism in which the relative proportions of phosphorylated and nonphosphorylated forms of a phosphotransferase constituent regulate the activity of the lactose permease.
磷酸烯醇丙酮酸 - 糖磷酸转移酶系统（PTS）对乳糖摄取的调节作用已在大肠杆菌ML 308 - 225菌株的膜泡中得到证实。磷酸转移酶系统的底物抑制了由D - 乳酸供能的乳糖摄取，但不抑制L - 丙氨酸或L - 脯氨酸的摄取。这种抑制作用可被囊泡内（而非囊泡外）的磷酸烯醇丙酮酸逆转。被电击导入囊泡的酶IIIglc制剂也抑制乳糖摄取，且这种抑制作用可被磷酸烯醇丙酮酸逆转。囊泡内的HPr和酶I刺激了α - 甲基糖苷的摄取，但不抑制或刺激乳糖积累。在0摄氏度下维持数天的囊泡部分丧失了：1）摄取乳糖的能力，2）积累PTS底物的能力，以及3）PTS介导的调节作用。添加磷酸烯醇丙酮酸可恢复所有这些活性。这些结果支持了一种机制，即磷酸转移酶成分的磷酸化和非磷酸化形式的相对比例调节乳糖通透酶的活性。
