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Antibiotic-induced replication stress triggers bacterial competence by increasing gene dosage near the origin

Jelle Slager1, Morten Kjos1, Laetitia Attaiech1

  • 1Molecular Genetics Group, Groningen Biomolecular Sciences and Biotechnology Institute, Centre for Synthetic Biology, University of Groningen, Nijenborgh 7, 9747 AG Groningen, the Netherlands.

Cell
|April 15, 2014
PubMed

Insights

Antibiotics targeting DNA replication activate bacterial competence by increasing gene copy number near the origin of replication (oriC). This conserved mechanism allows bacteria to respond to replication stress and potentially spread antibiotic resistance genes.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Streptococcus pneumoniae causes significant child mortality, with antibiotic resistance exacerbating the threat.
  • Antibiotic resistance genes spread rapidly in bacteria via DNA uptake (competence).
  • Competence can be triggered by certain antibiotics, suggesting an intrinsic bacterial response.

Purpose of the Study:

  • To elucidate the mechanism by which antibiotics activate bacterial competence.
  • To investigate the role of DNA replication and gene location in competence activation.

Main Methods:

  • Analysis of gene copy number changes in response to DNA replication-targeting antibiotics.
  • Transcriptome analyses to assess gene expression patterns.
  • Comparative analysis across different bacterial species.

Main Results:

  • Antibiotics targeting DNA replication increase the copy number of genes located near the origin of replication (oriC).
  • This increase in gene copy number activates competence initiation in Streptococcus pneumoniae.
  • Similar upregulation of origin-proximal gene expression was observed in other bacteria.
  • The mechanism is linked to replication fork stalling, a direct consequence of DNA replication stress.

Conclusions:

  • The location of competence genes near oriC facilitates a rapid response to replication stress.
  • Evolution has conserved this mechanism for robust bacterial adaptation.
  • This conserved pathway provides a potential target for combating antibiotic resistance spread.

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