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Updated: Jul 15, 2026

Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection
11:56

Nanomechanics of Drug-target Interactions and Antibacterial Resistance Detection

Published on: October 25, 2013

Role of insertion elements and yycFG in the development of decreased susceptibility to vancomycin in Staphylococcus

Andrea Jansen1, Michael Türck, Christiane Szekat

  • 1Institut für Medizinische Mikrobiologie, Immunologie und Parasitologie, Universitätsklinikum Bonn, Sigmund-Freud-Str. 25, D-53105 Bonn, Germany.

International Journal of Medical Microbiology : IJMM
|April 10, 2007
PubMed

Insights

Vancomycin resistance in Staphylococcus aureus involves the upregulation of the yycFG regulatory system and IS256 insertions. These genetic changes contribute to increased resistance in vancomycin-intermediate resistant S. aureus (VISA) strains.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Vancomycin is a critical glycopeptide antibiotic targeting bacterial cell wall synthesis.
  • Understanding vancomycin resistance mechanisms in Staphylococcus aureus is crucial for effective treatment.
  • Vancomycin intermediate-resistant Staphylococcus aureus (VISA) poses a significant clinical challenge.

Purpose of the Study:

  • To identify genes involved in vancomycin resistance in Staphylococcus aureus.
  • To analyze the expression profiles of vancomycin-resistant strains.
  • To investigate the role of genetic elements like IS256 in resistance.

Main Methods:

  • Gene expression profiling using a Staphylococcus aureus full-genome chip.
  • Sequencing of the yycFG promoter region.
  • Analysis of IS256 insertion and gene inactivation.
  • Population analyses of resistant strains.

Main Results:

  • The yycF (vicR) and yycG (vicK) two-component regulatory system was significantly upregulated in a VISA strain (SA137/93A).
  • An IS256 insertion in the yycFG promoter region of SA137/93A created a potentially stronger hybrid promoter.
  • In another VISA strain (SA137/93G), IS256 was found to inactivate the tcaA gene, contributing to increased resistance.

Conclusions:

  • The yycFG regulatory system plays a role in vancomycin resistance in S. aureus.
  • IS256 insertions, either in promoter regions or leading to gene inactivation (e.g., tcaA), are key mechanisms contributing to vancomycin and teicoplanin resistance.
  • Loss of SCCmec and tcaA inactivation contribute to increased resistance in VISA strains.

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