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Characterizing Multidrug Efflux Systems in Acinetobacter baumannii Using an Efflux-Deficient Bacterial Strain and a Single-Copy Gene Expression System
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Two-component regulatory systems in Pseudomonas aeruginosa: an intricate network mediating fimbrial and efflux pump

Melissa Sivaneson1, Helga Mikkelsen, Isabelle Ventre

  • 1Imperial College London, Division of Cell and Molecular Biology, Centre for Molecular Microbiology and Infection, South Kensington Campus, Flowers Building, SW7 2AZ London, UK.

Molecular Microbiology
|January 6, 2011
PubMed

Insights

Pseudomonas aeruginosa uses Roc systems to regulate biofilm formation and antibiotic resistance. These pathways coordinate fimbriae production and multidrug efflux pump activity, potentially adapting to the cystic fibrosis lung environment.

Area of Science:

  • Microbiology
  • Bacterial genetics
  • Signaling pathways

Background:

  • Pseudomonas aeruginosa causes chronic and acute infections.
  • Chronic infections involve fimbriae and biofilm formation.
  • The Roc1 two-component system regulates fimbriae assembly genes (cup genes).

Purpose of the Study:

  • Investigate the function of the uncharacterized roc2 gene cluster.
  • Elucidate cross-regulation between Roc1 and Roc2 signaling pathways.
  • Determine the role of Roc systems in Pseudomonas aeruginosa virulence and antibiotic resistance.

Main Methods:

  • Genetic analysis of roc1 and roc2 gene clusters.
  • Study of gene expression using reporter assays.
  • Analysis of antibiotic susceptibility in mutant strains.

Main Results:

  • Cross-regulation exists between Roc1 and Roc2 signaling pathways.
  • Sensors RocS2 and RocS1 converge on RocA1 to control cupC expression.
  • RocS2 and RocS1 act via RocA2 to repress mexAB-oprM genes, affecting antibiotic resistance.

Conclusions:

  • The Roc systems mediate cross-regulation impacting biofilm formation and antibiotic resistance.
  • Roc system activity correlates with P. aeruginosa adaptation in cystic fibrosis lungs.
  • Roc systems may sense and respond to the cystic fibrosis lung environment.

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