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Related Experiment Video

Updated: Jan 16, 2026

Quadruple-Checkerboard: A Modification of the Three-Dimensional Checkerboard for Studying Drug Combinations
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RecA Inhibitor Mitigates Bacterial Antibiotic Resistance.

Jin Ma1, Liwen Xu1, Keke Shang1

  • 1Key Laboratory of Functional Protein Research of Guangdong Higher Education Institutes and MOE Key Laboratory of Tumor Molecular Biology, Institute of Life and Health Engineering, Jinan University, Guangzhou 510632, China.

Microorganisms
|September 27, 2025
PubMed
Summary
This summary is machine-generated.

A new RecA inhibitor, BRITE-338733 (BR), effectively delays bacterial antibiotic resistance (AR) by targeting RecA-mediated pathways. This approach reduces tRNA upregulation, a key mechanism in early-stage AR development.

Keywords:
Escherichia coliRecARecA inhibitorbacterial resistancetRNAtranslation

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Area of Science:

  • Microbiology
  • Molecular Biology
  • Pharmacology

Background:

  • Bacterial antibiotic resistance (AR) is a major global health crisis.
  • Genome recombination enhances AR through mutations and gene transfer, often involving tRNA upregulation.
  • RecA protein is critical for bacterial genome recombination and DNA damage response.

Purpose of the Study:

  • To investigate the potential of RecA inhibitors to combat early-stage bacterial AR.
  • To evaluate the efficacy of BRITE-338733 (BR) as a RecA inhibitor against ciprofloxacin resistance in Escherichia coli.

Main Methods:

  • Subculturing Escherichia coli strain BW25113 with and without BRITE-338733 (BR) in the presence of ciprofloxacin.
  • Measuring tRNA levels and RecA expression.
  • Performing transcriptome sequencing to analyze cellular pathways affected by BR.

Main Results:

  • BRITE-338733 (BR) prevented ciprofloxacin resistance emergence up to the 7th generation.
  • BR treatment decreased tRNA levels and inhibited RecA expression upregulation.
  • Transcriptome analysis showed BR inhibits oxidative phosphorylation, electron transport, and translation, lowering bacterial energy and protein synthesis.
  • BR demonstrated safety for human cell viability at effective concentrations.

Conclusions:

  • BRITE-338733 (BR) effectively delays spontaneous antibiotic resistance by targeting RecA-mediated pathways.
  • Combining BR with antibiotics presents a novel strategy to counteract clinical AR, especially in early treatment stages.