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结核分枝杆菌中链霉素耐药性的分子基础:核糖体蛋白S12基因的改变及功能性16S核糖体RNA假结内的点突变

Molecular basis of streptomycin resistance in Mycobacterium tuberculosis: alterations of the ribosomal protein S12 gene and point mutations within a functional 16S ribosomal RNA pseudoknot.

作者信息

Finken M, Kirschner P, Meier A, Wrede A, Böttger E C

机构信息

Institut für Medizinische Mikrobiologie, Medizinische Hochschule Hannover, Germany.

出版信息

Mol Microbiol. 1993 Sep;9(6):1239-46. doi: 10.1111/j.1365-2958.1993.tb01253.x.

DOI:10.1111/j.1365-2958.1993.tb01253.x
PMID:7934937
Abstract

Multidrug-resistant strains of Mycobacterium tuberculosis have resulted in several recent outbreaks. Recognition of drug resistance is important both for treatment and to prevent further transmission. Here we use molecular biology techniques to study the basis of streptomycin resistance in single and multidrug-resistant M. tuberculosis. We demonstrate that streptomycin resistance is associated with mutations implicated in ribosomal resistance. The mutations found either lead to amino acid changes in ribosomal protein S12 or alter the primary structure of the 16S rRNA. The 16S rRNA region mutated perturbs a pseudoknot structure in a region which has been linked to ribosomal S12 protein.

摘要

结核分枝杆菌的多重耐药菌株导致了近期的几起疫情爆发。识别耐药性对于治疗和防止进一步传播都很重要。在此,我们使用分子生物学技术来研究单耐药和多耐药结核分枝杆菌中链霉素耐药性的基础。我们证明链霉素耐药性与核糖体耐药相关的突变有关。所发现的突变要么导致核糖体蛋白S12中的氨基酸变化,要么改变16S rRNA的一级结构。发生突变的16S rRNA区域扰乱了与核糖体S12蛋白相关区域的假结结构。

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