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Published on: September 8, 2021

Intact mutS in laboratory-derived and clinical glycopeptide-intermediate Staphylococcus aureus strains

Arunachalam Muthaiyan1, Radheshyam K Jayaswal, Brian J Wilkinson

  • 1Microbiology Group, Department of Biological Sciences, Illinois State University, Normal, Illinois 61790-4120, USA.

Antimicrobial Agents and Chemotherapy
|January 27, 2004
PubMed

Insights

Mutations in the mutS gene did not cause vancomycin resistance in Staphylococcus aureus strains. Sequencing confirmed the mutS gene was intact in all parent and intermediate strains studied.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Staphylococcus aureus is a significant pathogen.
  • Vancomycin is a critical antibiotic for treating S. aureus infections.
  • The development of vancomycin resistance in S. aureus is a major public health concern.

Purpose of the Study:

  • To investigate the role of the mutS gene in the development of vancomycin resistance in Staphylococcus aureus.
  • To determine if mutations in the mutS gene are associated with vancomycin intermediate resistance.

Main Methods:

  • Sequencing of the mutS gene.
  • Analysis of 10 parent and glycopeptide-intermediate Staphylococcus aureus strains.

Main Results:

  • The mutS gene was found to be intact in all 10 strains analyzed.
  • No mutations were identified in the mutS gene in either parent or vancomycin-intermediate strains.

Conclusions:

  • Mutations in the mutS gene are not responsible for the development of vancomycin resistance in the studied Staphylococcus aureus strains.
  • The methyl-directed mismatch repair system, as assessed by the mutS gene, does not appear to be involved in the emergence of vancomycin resistance in these strains.

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