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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.
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Trchоunian et al. (1999) studied this question.
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