Background/Objective: The anti-restriction protein ArdA-H1, found in multiresistant
Staphylococcus aureus (MRSA) strains from the ST239-SCC
mecIII lineage, inhibits restriction–modification systems, fostering horizontal gene transfer (HGT) and supporting genetic adaptability and resistance. This study investigates the regulatory mechanisms controlling
ardA-H1 expression
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Background/Objective: The anti-restriction protein ArdA-H1, found in multiresistant
Staphylococcus aureus (MRSA) strains from the ST239-SCC
mecIII lineage, inhibits restriction–modification systems, fostering horizontal gene transfer (HGT) and supporting genetic adaptability and resistance. This study investigates the regulatory mechanisms controlling
ardA-H1 expression in
S. aureus under various stress conditions, including acidic pH, iron limitation, and vancomycin exposure, and explores the roles of the Agr quorum sensing system.
Methods: The expression of
ardA-H1 was analyzed in
S. aureus strains exposed to environmental stressors using real-time quantitative reverse transcription PCR. Comparisons were made between Agr-functional and Agr-deficient strains. In addition, Agr inhibition was achieved using a heterologous Agr autoinducing peptide.
Results: The Agr system upregulated
ardA-H1 expression in acidic and iron-limited conditions. However, vancomycin induced
ardA-H1 activation specifically in the Agr-deficient strain GV69, indicating that an alternative regulatory pathway controls
ardA-H1 expression in the absence of
agr. The vancomycin response in GV69 suggests that diminished quorum sensing may offer a survival advantage by promoting persistence and HGT-related adaptability.
Conclusion: Overall, our findings provide new insights into the intricate relationships between quorum-sensing, stress responses, bacterial virulence, and genetic plasticity, enhancing our understanding of
S.
aureus adaptability in challenging environments.
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