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PBP4 Mediates β-Lactam Resistance by Altered Function.

Som S Chatterjee1, Liang Chen2, Aubre Gilbert3

  • 1Division of HIV/AIDS, Infectious Diseases and Global Health, Department of Medicine, University of California, San Francisco, San Francisco General Hospital, San Francisco, California, USA som.chatterjee@ucsf.edu.

Antimicrobial Agents and Chemotherapy
|August 16, 2017
PubMed
Summary
This summary is machine-generated.

Penicillin binding protein 4 (PBP4) mutations in Staphylococcus aureus enhance resistance to beta-lactams. Missense mutations directly aid resistance, while promoter mutations increase PBP4 levels, suggesting cooperative effects among penicillin-binding proteins.

Keywords:
PBP4Staphylococcus aureusβ-lactam resistance

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Antimicrobial Resistance

Background:

  • Staphylococcus aureus is a major human pathogen.
  • Beta-lactam antibiotics are crucial for treating S. aureus infections.
  • Emergence of antibiotic resistance in S. aureus poses a significant public health threat.

Purpose of the Study:

  • To investigate the role of Penicillin Binding Protein 4 (PBP4) in mediating high-level beta-lactam resistance in Staphylococcus aureus.
  • To identify specific mutations in the pbp4 gene associated with this resistance.
  • To elucidate the mechanisms by which these mutations confer resistance.

Main Methods:

  • Genomic analysis of beta-lactam resistant Staphylococcus aureus strains.
  • Identification and characterization of missense and promoter mutations in the pbp4 gene.
  • Functional studies to assess the impact of mutations on PBP4 activity and beta-lactam resistance levels.

Main Results:

  • Several missense and promoter mutations in pbp4 were identified in resistant strains.
  • Missense mutations were shown to directly enhance the beta-lactam resistance function of PBP4.
  • Promoter mutations resulted in the overexpression of pbp4, contributing to increased resistance.
  • Evidence suggests a synergistic interaction between PBP4 and other penicillin-binding proteins (PBPs) in conferring resistance.

Conclusions:

  • PBP4 plays a significant role in high-level beta-lactam resistance in Staphylococcus aureus.
  • Both direct functional alterations (missense mutations) and increased expression (promoter mutations) of PBP4 contribute to resistance.
  • The findings highlight a potential cooperative mechanism among PBPs in mediating antibiotic resistance, offering new insights for therapeutic strategies.