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金黄色葡萄球菌噬菌体抗性突变体中肽聚糖与磷壁酸之间连接单元生物合成的缺陷。

Defect in biosynthesis of the linkage unit between peptidoglycan and teichoic acid in a bacteriophage-resistant mutant of Staphylococcus aureus.

作者信息

Bracha R, Davidson R, Mirelman D

出版信息

J Bacteriol. 1978 May;134(2):412-7. doi: 10.1128/jb.134.2.412-417.1978.

Abstract

The biosynthesis of the linkage region between peptidoglycan and the ribitol teichoic acid was investigated in the bacteriophage-resistant, teichoic acid-less mutant Staphylococcus aureus 52A5 (Chatterjee et al., J. Bacteriol. 100:846--853, 1969). Membrane preparations of this strain were found to be incapable of forming the first intermediate of the biosynthetic pathway, namely, the transfer of N-acetyl-D-glucosamine (GlcNAc) from UDP-GlcNAc to the acceptor molecule, which presumbably is undecaprenol phosphate (R. Bracha and L. Glaser, Biochem. Biophys. Res. Commun. 72:1091--1098, 1976). The addition of heat-inactivated membrane preparations of S. aureus 52A2 (which normally has ribitol teichoic acid) that had been preincubated with UDP-GlcNAc to membranes of strain 52A5 enabled the synthesis of teichoic acid. These data suggest that the mutational defect in the teichoic acid-less organism is in the synthesis of the first compound of the linkage unit, and this is apparently the reason for its absence in the cell walls.

摘要

在抗噬菌体、无磷壁酸的金黄色葡萄球菌突变株52A5中研究了肽聚糖与核糖醇磷壁酸之间连接区域的生物合成(Chatterjee等人,《细菌学杂志》100:846 - 853,1969年)。发现该菌株的膜制剂无法形成生物合成途径的第一个中间体,即将N - 乙酰 - D - 葡糖胺(GlcNAc)从UDP - GlcNAc转移到受体分子,该受体分子可能是十一异戊烯醇磷酸(R. Bracha和L. Glaser,《生物化学与生物物理研究通讯》72:1091 - 1098,1976年)。将预先与UDP - GlcNAc预孵育的金黄色葡萄球菌52A2(通常含有核糖醇磷壁酸)的热灭活膜制剂添加到52A5菌株的膜中,能够合成磷壁酸。这些数据表明,无磷壁酸生物体中的突变缺陷在于连接单元第一种化合物的合成,这显然是其在细胞壁中不存在的原因。

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