Damadian R
J Bacteriol. 1968 Jan;95(1):113-22. doi: 10.1128/jb.95.1.113-122.1968.
A potassium transport mutant of Escherichia coli is described which is deficient in the intake of potassium. The phenotype of this mutant is characterized by (i) failure to grow in K(+)-deficient medium, (ii) failure to accumulate K(+) in K(+)-deficient medium, (iii) a steady-state intracellular K(+) that varies sigmoidally with the medium K(+) concentration, (iv) a signoidally shaped rate-concentration curve and a curved reciprocal plot for net K(+) uptake kinetics, and (v) a low steady-state flux of potassium associated with a reduced influx rate constant. The data are discussed in terms of the present day models of cation transport. These models have led to four possible explanations of the mutant's phenotype: (i) a selectivity reversal such that intracellular cation binding sites bind another cation instead of K(+); (ii) a structural alteration of cation binding cell proteins so that K(+) is bound by "cooperative binding" (sigmoid isotherm) instead of by simple adsorption (hyperbolic isotherm); (iii) conversion of an enzyme in intermediate metabolism that rate-limits K(+) uptake to an allosteric protein; (iv) conversion of the "carrier protein" for K(+) to an allosteric protein.
描述了一种大肠杆菌的钾转运突变体,其钾摄入存在缺陷。该突变体的表型特征为:(i) 在低钾培养基中无法生长;(ii) 在低钾培养基中无法积累钾;(iii) 稳态细胞内钾浓度随培养基钾浓度呈S形变化;(iv) 净钾摄取动力学的速率-浓度曲线呈S形,双倒数图呈曲线;(v) 钾的稳态通量较低,伴有流入速率常数降低。根据当前的阳离子转运模型对数据进行了讨论。这些模型对突变体表型提出了四种可能的解释:(i) 选择性逆转,使得细胞内阳离子结合位点结合另一种阳离子而非钾;(ii) 阳离子结合细胞蛋白的结构改变,使得钾通过“协同结合”(S形等温线)而非简单吸附(双曲线等温线)结合;(iii) 将中间代谢中限速钾摄取的一种酶转化为别构蛋白;(iv) 将钾的“载体蛋白”转化为别构蛋白。