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A Fluorescence-based Method to Study Bacterial Gene Regulation in Infected Tissues
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Tn551-mediated insertional inactivation of the fmtB gene encoding a cell wall-associated protein abolishes

H Komatsuzawa1, K Ohta, M Sugai

  • 1Department of Microbiology, Hiroshima University School of Dentistry, Japan. hkomatsu@ipc.hiroshima-u.ac.jp

The Journal of Antimicrobial Chemotherapy
|July 15, 2000
PubMed

Insights

A novel gene, fmtB, was identified in methicillin-resistant Staphylococcus aureus (MRSA). Inactivating fmtB reduces resistance to oxacillin, suggesting a new target for combating MRSA infections.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Methicillin-resistant Staphylococcus aureus (MRSA) poses a significant public health threat due to its resistance to antibiotics.
  • Understanding the genetic basis of MRSA resistance is crucial for developing new therapeutic strategies.

Purpose of the Study:

  • To investigate the role of the fmtB gene in the oxacillin resistance of MRSA.
  • To elucidate the mechanism by which fmtB influences antibiotic resistance.

Main Methods:

  • Tn551 mutagenesis was used to identify genes affecting oxacillin resistance in MRSA.
  • Gene mapping, protein analysis, and complementation studies were performed.
  • Immunoblotting was used to confirm protein localization.

Main Results:

  • Tn551 insertion in fmtB reduced oxacillin and Triton X-100 resistance in MRSA strains.
  • The fmtB gene encodes a cell wall-localized protein.
  • Overexpression of the downstream glmM gene or addition of glucosamine restored oxacillin resistance in fmtB mutants.

Conclusions:

  • The fmtB gene plays an indirect role in MRSA oxacillin resistance.
  • Inactivation of fmtB affects cell wall precursor synthesis, which can be compensated by increasing glucosamine-1-phosphate production.

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