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Updated: Jun 28, 2025

A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues
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A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues

Published on: February 19, 2019

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Prophage-encoded methyltransferase drives adaptation of community-acquired methicillin-resistant Staphylococcus

Robert J Ulrich1, Magdalena Podkowik1,2, Rebecca Tierce3

  • 1Department of Medicine, NYU Grossman School of Medicine, New York, NY, USA.

Biorxiv : the Preprint Server for Biology
|April 25, 2024
PubMed

Insights

A novel mechanism of Staphylococcus aureus virulence involves epigenetic regulation. A phage-encoded enzyme, pamA, increases skin abscess size by upregulating fibronectin-binding protein A (fnbA), promoting biofilm formation.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) USA300 has evolved variants.
  • Prophage acquisition, specifically mosaic Φ11 (mΦ11), is linked to increased virulence in CA-MRSA skin infections.

Purpose of the Study:

  • To elucidate the mechanism by which the mΦ11 prophage enhances CA-MRSA virulence in skin infections.
  • To identify the specific genes and pathways involved in mΦ11-mediated virulence.

Main Methods:

  • Investigated the role of mΦ11-encoded adenine methyltransferase (pamA) in virulence.
  • Assessed the impact of pamA on fibronectin-binding protein A (fnbA) expression.
  • Examined the effect of pamA and fnbA inactivation on abscess size and inflammation in vivo.
  • Analyzed the role of pamA in promoting biofilm formation within skin abscesses.

Main Results:

  • Abscess size and skin inflammation correlated with the DNA methylase activity of pamA.
  • pamA significantly increased the expression of fnbA.
  • Inactivation of fnbA abolished pamA's effect on virulence, confirming fnbA as a pamA-specific virulence factor.
  • pamA was shown to promote in vivo biofilm formation in skin abscesses, mediated by FnBPA.

Conclusions:

  • Phage mΦ11 regulates Staphylococcus aureus virulence through epigenetic modification via pamA.
  • pamA enhances virulence by upregulating fnbA, which promotes biofilm formation in skin abscesses.
  • This study reveals a novel mechanism of phage-mediated virulence regulation through epigenetic control of staphylococcal gene expression.

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