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Updated: Jun 13, 2025

Stress-induced Antibiotic Susceptibility Testing on a Chip
Published on: January 8, 2014
Staphylococcus aureus Stress Response to Bicarbonate Depletion
Elisa Liberini1, Sook-Ha Fan1,2, Arnold S Bayer2,3
1Microbial Genetics, Interfaculty Institute of Microbiology and Infection Medicine Tübingen (IMIT), University of Tübingen, 72076 Tübingen, Germany.
Bicarbonate deficiency in Staphylococcus aureus causes significant cell wall thickening and altered glycosylation, leading to increased resistance against lysostaphin and Triton X-100. This stress response impacts bacterial resilience.
Area of Science:
- Microbiology
- Bacterial Physiology
- Cell Wall Biology
Background:
- Bicarbonate and CO2 are vital for bacterial carboxylation.
- Staphylococcus aureus relies on the MpsABC transporter for carbon concentration.
- mpsABC deletion mutants exhibit impaired growth in ambient air.
Purpose of the Study:
- To investigate cellular and molecular changes in S. aureus under CO2/bicarbonate deficiency.
- To understand the mechanisms behind the observed resistance in the mutant strain.
- To analyze the impact of carbon limitation on S. aureus cell wall composition and gene expression.
Main Methods:
- Electron microscopy to assess cell wall thickness.
- Mass spectrometry for muropeptide analysis.
- Flow cytometry for wall teichoic acid (WTA) glycosylation profiling.
- Comparative transcriptome analysis.
Main Results:
- The ΔmpsABC mutant displayed a twofold thicker cell wall.
- Mutant cells showed resistance to lysostaphin and Triton X-100.
- Alanine incorporation into pentaglycine bridges conferred lysostaphin resistance.
- Altered WTA glycosylation (less alpha, more beta) explained Triton X-100 resistance.
- Upregulation of autolysin genes (e.g., sceD) and downregulation of cell wall-anchored proteins, secreted proteins, transporters, and toxins.
Conclusions:
- Bicarbonate deficiency acts as a stressor in S. aureus.
- This stress induces significant changes in cell wall composition.
- Global gene expression is altered, contributing to enhanced resilience.
- The study elucidates a novel stress response mechanism impacting bacterial survival.
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