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Transcriptomic and functional analysis of NaCl-induced stress in Enterococcus faecalis
Margrete Solheim1, Sabina Leanti La Rosa1, Thomas Mathisen1
1Laboratory of Microbial Gene Technology and Food Microbiology, The Norwegian University of Life Sciences, Ås, Norway.
Plos One
|April 24, 2014
Summary
Enterococcus faecalis utilizes the enterococcal polysaccharide antigen (epa) to enhance its resistance to salt stress. This epa locus also improves tolerance to other cell envelope stressors, potentially linking its robustness to virulence.
Area of Science:
- Microbiology
- Molecular Biology
- Pathogenesis
Background:
- Enterococcus faecalis exhibits robust physiology, enabling tolerance to diverse environmental stresses.
- Understanding stress responses is crucial for elucidating E. faecalis pathogenesis and persistence.
Purpose of the Study:
- To investigate the transcriptional response of E. faecalis V583 to high salt (6.5% NaCl) conditions.
- To determine the role of the enterococcal polysaccharide antigen (epa) locus in salt stress resistance and virulence.
Main Methods:
- Transcriptional profiling of E. faecalis V583 exposed to high NaCl.
- Construction and analysis of epaB and epaE mutants.
- Complementation studies to validate gene function.
- Assessment of resistance to various cell envelope stressors.
Main Results:
- High salt induced genes for potassium and glycine betaine uptake, chaperones, and the epa locus.
- Mutants lacking epaB or epaE showed reduced salt stress resistance.
- Epa conferred increased resistance to multiple cell envelope stress-inducing factors.
- High salt repressed the gelE-sprE operon, impairing gelatinase activity.
Conclusions:
- The epa locus plays a significant role in E. faecalis salt stress resistance and overall physiological robustness.
- Epa contributes to virulence by enhancing resistance to cell envelope stressors.
- High salt concentrations antagonize GBAP-pheromone dependent induction of the gelE-sprE operon.
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