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野生型和突变型粪肠球菌中砷酸盐与磷酸盐转运系统的相互作用

Interaction of arsenate with phosphate-transport systems in wild- type and mutant Streptococcus faecalis.

作者信息

Harold F M, Baarda J R

出版信息

J Bacteriol. 1966 Jun;91(6):2257-62. doi: 10.1128/jb.91.6.2257-2262.1966.

Abstract

Harold, F. M. (National Jewish Hospital, Denver, Colo.), and J. R. Baarda. Interaction of arsenate with phosphate-transport systems in wild-type and mutant Streptococcus faecalis. J. Bacteriol. 91:2257-2262. 1966.-Arsenate competitively inhibits the growth of Streptococcus faecalis, primarily by competition with phosphate for a common transport system. Arsenate is itself accumulated by the cells; the uptake requires metabolic energy, and the intracellular arsenate level may reach 0.01 m. Cells loaded with arsenate have lost the capacity to take up radioactive glutamate, rubidium, phosphate, or arsenate itself, apparently by the uncoupling of adenosine triphosphate generation. The pH dependence of arsenate uptake is complex. At low concentrations of extracellular arsenate, uptake by the wild-type strain 9790 exhibits a single maximum about pH 8; mutant PT-1, previously shown to be defective in phosphate uptake, takes up essentially no arsenate. At high concentrations of arsenate, uptake by the wild type is bimodal with maxima at pH 5.5 and 9; the uptake curve for mutant PT-1 corresponds to the shoulder in the curve for the wild type. The apparent dissociation constant for arsenate uptake by the wild type is approximately 10(-5)m from pH 5 to 9, whereas that for mutant PT-1 is about 5 x 10(-5) M at pH 5 and rises rapidly with increasing pH. The results confirm the earlier conclusion that the lesion in mutant PT-1 resides in the transport of phosphate and arsenate. It is proposed that the wild type has two distinct transport systems, whereas the mutant has lost the one with alkaline pH optimum.

摘要

哈罗德,F.M.(科罗拉多州丹佛市国家犹太医院)和J.R.巴尔达。野生型和突变型粪肠球菌中砷酸盐与磷酸盐转运系统的相互作用。《细菌学杂志》91:2257 - 2262。1966年。——砷酸盐竞争性抑制粪肠球菌的生长,主要是通过与磷酸盐竞争共同的转运系统。砷酸盐本身会被细胞积累;摄取需要代谢能量,细胞内砷酸盐水平可达0.01 m。装载有砷酸盐的细胞失去了摄取放射性谷氨酸、铷、磷酸盐或砷酸盐本身的能力,显然是由于三磷酸腺苷生成的解偶联。砷酸盐摄取的pH依赖性很复杂。在细胞外砷酸盐浓度较低时,野生型菌株9790的摄取在pH约8处呈现单一最大值;先前已证明在磷酸盐摄取方面有缺陷的突变体PT - 1基本上不摄取砷酸盐。在高浓度砷酸盐时,野生型的摄取呈双峰,在pH 5.5和9处有最大值;突变体PT - 1的摄取曲线与野生型曲线的肩部相对应。野生型摄取砷酸盐的表观解离常数在pH 5至9时约为10(-5)m,而突变体PT - 1在pH 5时约为5×10(-5)M,并随pH升高而迅速上升。结果证实了早期的结论,即突变体PT - 1的损伤在于磷酸盐和砷酸盐的转运。有人提出野生型有两种不同的转运系统,而突变体失去了最适pH为碱性的那种转运系统。

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