Related Experiment Video

Updated: Jun 19, 2026

Time-Lapse Epifluorescence Microscopy Imaging of Pseudomonas aeruginosa and Staphylococcus aureus Heterogeneous Phenotypes
07:44

Time-Lapse Epifluorescence Microscopy Imaging of Pseudomonas aeruginosa and Staphylococcus aureus Heterogeneous Phenotypes

Published on: February 14, 2025

Phenotypic changes in ciprofloxacin-resistant Staphylococcus aureus

Lili R Mesak1, Julian Davies

  • 1Department of Microbiology and Immunology, University of British Columbia, Life Sciences Institute, 2350 Health Science Mall, Vancouver, BC V6T1Z3, Canada.

Research in Microbiology
|October 13, 2009
PubMed

Insights

Subinhibitory antibiotic concentrations, including moxifloxacin, activate DNA repair genes and increase mutation rates in Staphylococcus aureus. This study investigates phenotypic changes and norA gene expression in resistant strains.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Subinhibitory antibiotic concentrations can influence bacterial gene expression and mutation rates.
  • Staphylococcus aureus is a significant human pathogen, and understanding its response to antibiotics is crucial for treatment.
  • Previous studies have explored the effects of antibiotics on SOS and DNA repair in S. aureus.

Purpose of the Study:

  • To investigate the impact of subinhibitory concentrations of mitomycin C and moxifloxacin on SOS and DNA repair gene expression in Staphylococcus aureus.
  • To examine phenotypic alterations in ciprofloxacin-resistant (Cip(r)) S. aureus strains with mutations in fluoroquinolone resistance targets.
  • To assess the effect of these antibiotics on norA gene expression and mutation rates in S. aureus.

Main Methods:

  • Gene expression analysis of SOS response genes (lexA, recA, sosA, umuC).
  • Biolog Phenotype MicroArrays to evaluate phenotypic changes in resistant strains.
  • Quantitative analysis of norA gene expression in response to antibiotics.
  • Mutation rate determination in S. aureus.

Main Results:

  • Mitomycin C and moxifloxacin induced SOS response genes in a ciprofloxacin-resistant S. aureus strain.
  • Phenotypic changes in resistant strains were assessed using Biolog Phenotype MicroArrays.
  • Overexpression of the norA gene was observed in Cip(r) strains treated with mitomycin C and moxifloxacin.
  • Subinhibitory concentrations of ciprofloxacin were confirmed to increase mutation rates in S. aureus.

Conclusions:

  • Subinhibitory concentrations of certain antibiotics can trigger DNA repair mechanisms and alter gene expression in Staphylococcus aureus.
  • Fluoroquinolone resistance mechanisms and their impact on bacterial phenotypes and gene expression are complex.
  • Understanding these responses is vital for developing effective strategies against antibiotic-resistant bacteria.

More Related Videos

Metabolic Profiling to Determine Bactericidal or Bacteriostatic Effects of New Natural Products using Isothermal Microcalorimetry07:28

Metabolic Profiling to Determine Bactericidal or Bacteriostatic Effects of New Natural Products using Isothermal Microcalorimetry

Published on: October 29, 2020

Related Concept Videos

Mechanism of Antibiotic Resistance in MRSA01:25

Mechanism of Antibiotic Resistance in MRSA

Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and acquisition...
Clinical Significance of Antibiotic Resistance01:25

Clinical Significance of Antibiotic Resistance

Methicillin-resistant Staphylococcus aureus (MRSA) presents a critical public health threat, arising from its capacity to resist β-lactam antibiotics due to acquisition of the mecA gene within the staphylococcal cassette chromosome mec (SCCmec). This gene encodes penicillin-binding protein 2a (PBP2a), which impairs binding efficacy of methicillin and other β-lactams. MRSA has evolved into distinct clonal lineages impacting humans and animals alike, reinforcing its significance within the One...
Development of Antibiotic Resistance01:30

Development of Antibiotic Resistance

Antibiotic resistance is a major public health concern that arises when bacteria evolve mechanisms to withstand the effects of antibiotic treatments. This resistance can be intrinsic, acquired through genetic mutations, or transferred between bacteria via horizontal gene transfer. The development of antibiotic resistance poses significant challenges in treating bacterial infections and necessitates ongoing research to develop new therapeutic strategies.Intrinsic resistance occurs when bacterial...
Staphylococcal Skin Infections01:29

Staphylococcal Skin Infections

Staphylococcus aureus is a Gram-positive coccus that resides harmlessly on the skin and mucous membranes of healthy individuals. When the skin barrier is breached, it can shift from a commensal to an opportunistic pathogen. This transition is facilitated by surface adhesins, such as clumping factor B and S. aureus surface protein G (SasG), which bind to structural proteins, including loricrin and cytokeratin, in the damaged epidermis. Protein A, another key factor, binds the Fc region of...
Inhibitors of Bacterial DNA Synthesis01:28

Inhibitors of Bacterial DNA Synthesis

Bacterial pathogens depend on precise and efficient DNA replication to sustain infection. Two type II topoisomerases—DNA gyrase and topoisomerase IV—are critical to this process, as they resolve DNA supercoiling and unlink chromosomes during replication. Fluoroquinolones, synthetic derivatives of quinolones, exploit this mechanism by stabilizing the transient DNA–enzyme cleavage complex, preventing strand religation, and causing lethal double-strand breaks. These antibiotics are selectively...