Trchounian A, Kobayashi H
Faculty of Pharmaceutical Sciences, Chiba University, Japan.
FEBS Lett. 1999 Mar 26;447(2-3):144-8. doi: 10.1016/s0014-5793(99)00288-4.
The K+ uptake was observed in washed cells of Escherichia coli, wild-type, upon hyper-osmotic stress at pH 5.5 when glucose was supplemented. This uptake had apparent a Km of 0.58 mM and Vmax of 0.10 micromol K+/min/mg protein. Such a K+ uptake was investigated using a mutant defective in Kdp and TrkA but with a functional Kup and a mutant defective in Kdp and Kup but having an active TrkA. The K+ uptake to reach the steady state level as well as the initial K+ influx rate in the first mutant were at least 3.5-fold greater than these values with the second mutant and similar to those of the wild-type. Such differences in the K+ uptake activity were correlated with K+ requirements for growth of these mutants. Moreover, the K+ uptake in the wild-type was blocked by a protonophore (carbonyl cyanide m-chlorophenylhydrazone). Valinomycin, arsenate and N,N'-dicyclohexylcarbodiimide were not effective in changing the K+ uptake. It is suggested that Kup is the major K+ uptake system in E. coli upon hyper-osmotic stress at a low pH.
在pH 5.5且添加葡萄糖的情况下，对野生型大肠杆菌的洗涤细胞施加高渗胁迫时，观察到了钾离子（K⁺）的摄取。这种摄取的表观Km为0.58 mM，Vmax为0.10微摩尔K⁺/分钟/毫克蛋白质。使用Kdp和TrkA缺陷但Kup功能正常的突变体以及Kdp和Kup缺陷但TrkA活性正常的突变体对这种K⁺摄取进行了研究。第一个突变体中达到稳态水平的K⁺摄取以及初始K⁺流入速率比第二个突变体的值至少高3.5倍，且与野生型相似。K⁺摄取活性的这种差异与这些突变体生长对K⁺的需求相关。此外，野生型中的K⁺摄取被质子载体（羰基氰化物间氯苯腙）阻断。缬氨霉素、砷酸盐和N,N'-二环己基碳二亚胺对改变K⁺摄取无效。这表明在低pH下的高渗胁迫下，Kup是大肠杆菌中主要的K⁺摄取系统。
