A multidrug resistance plasmid contains the molecular switch for type VI secretion in Acinetobacter baumannii

Brent S Weber1, Pek Man Ly2, Joshua N Irwin2

  • 1Department of Biological Sciences, University of Alberta, Edmonton, AB, Canada T6G 2G2; Department of Molecular Microbiology, Washington University School of Medicine in St. Louis, St. Louis, MO 63110;

Insights

Multidrug-resistant Acinetobacter baumannii uses a resistance plasmid to control its type VI secretion system (T6SS). Plasmid loss activates T6SS to kill competitors, but increases antibiotic susceptibility in these superbug infections.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Acinetobacter baumannii is a problematic multidrug-resistant pathogen with increasing infection rates.
  • This bacterium possesses a type VI secretion system (T6SS) for interbacterial competition.
  • Regulatory mechanisms governing T6SS expression in A. baumannii remain largely unknown.

Purpose of the Study:

  • To investigate the regulatory mechanisms controlling type VI secretion system (T6SS) expression in multidrug-resistant Acinetobacter baumannii.
  • To understand the role of resistance plasmids in the regulation of T6SS activity.

Main Methods:

  • Analysis of multidrug-resistant Acinetobacter baumannii strains.
  • Plasmid characterization and identification of genetic elements.
  • Assessment of T6SS activity and antibiotic susceptibility.

Main Results:

  • Multidrug-resistant A. baumannii strains harbor self-transmissible plasmids encoding negative regulators of the T6SS.
  • T6SS activity is silenced in plasmid-carrying, antibiotic-resistant cells.
  • Plasmid loss leads to T6SS activation, bacterial killing, and increased antibiotic susceptibility.

Conclusions:

  • A resistance plasmid regulates T6SS activity in A. baumannii, influencing bacterial competition and antibiotic resistance.
  • Plasmid-mediated regulation contributes to cell differentiation, with some cells specialized for killing competitors at the cost of antibiotic susceptibility.
  • This mechanism highlights a novel role for resistance plasmids in bacterial population dynamics and virulence.

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