对临床耐万古霉素金黄色葡萄球菌分离株的微阵列转录分析。
Microarray transcription analysis of clinical Staphylococcus aureus isolates resistant to vancomycin.
作者信息
Mongodin Emmanuel, Finan Jon, Climo Michael W, Rosato Adriana, Gill Steven, Archer Gordon L
机构信息
Department of Medicine, Medical College of Virginia at Virginia Commonwealth University and the Hunter Holmes McGuire Veterans Affairs Medical Center, Richmond, Virginia, USA.
出版信息
J Bacteriol. 2003 Aug;185(15):4638-43. doi: 10.1128/JB.185.15.4638-4643.2003.
Abstract
The transcriptomes of vancomycin intermediate-resistance Staphylococcus aureus (VISA) clinical isolates HIP5827 and Mu50 (MIC = 8 micro g/ml) were compared to those of highly vancomycin-resistant S. aureus (VRSA; MIC = 32 micro g/ml) passage derivatives by microarray. There were 35 genes with increased transcription and 16 genes with decreased transcription in common between the two VRSAs compared to those of their VISA parents. Of the 35 genes with increased transcription, 15 involved purine biosynthesis or transport, and the regulator (purR) of the major purine biosynthetic operon (purE-purD) was mutant. We hypothesize that increased energy (ATP) is required to generate the thicker cell walls that characterize resistant mutants.
摘要
通过微阵列比较了万古霉素中介耐药金黄色葡萄球菌（VISA）临床分离株HIP5827和Mu50（MIC = 8μg/ml）与高耐万古霉素金黄色葡萄球菌（VRSA；MIC = 32μg/ml）传代衍生物的转录组。与它们的VISA亲本相比，两个VRSA之间共有35个基因转录增加，16个基因转录减少。在转录增加的35个基因中，15个涉及嘌呤生物合成或转运，主要嘌呤生物合成操纵子（purE-purD）的调节因子（purR）发生了突变。我们推测，产生耐药突变体特征性的更厚细胞壁需要增加能量（ATP）。
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