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Microarray transcription analysis of clinical Staphylococcus aureus isolates resistant to vancomycin
Emmanuel Mongodin1, Jon Finan, Michael W Climo
1Department of Medicine, Medical College of Virginia at Virginia Commonwealth University and the Hunter Holmes McGuire Veterans Affairs Medical Center, Richmond, Virginia, USA.
Journal of Bacteriology
|July 18, 2003
Summary
Vancomycin-resistant Staphylococcus aureus (VRSA) exhibits altered gene expression, particularly in purine metabolism, potentially linked to thicker cell walls. This suggests increased energy demands contribute to vancomycin resistance in bacteria.
Area of Science:
- Microbiology
- Genomics
- Molecular Biology
Background:
- Staphylococcus aureus can develop resistance to vancomycin, a critical antibiotic.
- Vancomycin intermediate-resistance S. aureus (VISA) and vancomycin-resistant S. aureus (VRSA) represent increasing clinical challenges.
Purpose of the Study:
- To compare the transcriptomes of VISA and VRSA strains.
- To identify common genetic alterations associated with high-level vancomycin resistance.
Main Methods:
- Microarray analysis was used to compare gene transcription profiles.
- Clinical isolates HIP5827 and Mu50 (VISA) were compared to their VRSA passage derivatives.
Main Results:
- 35 genes showed increased transcription and 16 genes showed decreased transcription in common between VRSA and VISA strains.
- Of the upregulated genes, 15 were involved in purine biosynthesis or transport.
- A mutation in the purine regulator (purR) of the purine biosynthetic operon was observed.
Conclusions:
- Increased purine biosynthesis and potential energy demands (ATP) may be linked to the thicker cell walls characteristic of VRSA.
- Transcriptomic analysis reveals key metabolic pathways altered in high-level vancomycin resistance.