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MexT functions as a redox-responsive regulator modulating disulfide stress resistance in Pseudomonas aeruginosa

Emilie Fargier1, Micheál Mac Aogáin, Marlies J Mooij

  • 1BIOMERIT Research Centre, Department of Microbiology, University College Cork, Cork, Ireland.

Journal of Bacteriology
|May 1, 2012
PubMed

Insights

The LysR regulator MexT in Pseudomonas aeruginosa controls disulfide stress resistance. Inactivation of MexT increases susceptibility to diamide, implicating MexT in redox homeostasis and the MexEF-OprN efflux system.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Biochemistry

Background:

  • MexT is a known regulator of antibiotic resistance and virulence in Pseudomonas aeruginosa.
  • Its role in intrinsic stress resistance, particularly disulfide stress, was previously unidentified.

Purpose of the Study:

  • To investigate the novel role of MexT in mediating intrinsic disulfide stress resistance in Pseudomonas aeruginosa.
  • To elucidate the mechanism by which MexT influences cellular redox control and stress response.

Main Methods:

  • Phenotypic analysis of mexT mutants for susceptibility to disulfide stress elicitors like diamide.
  • Transcriptional analysis of MexT-regulated genes, including the MexEF-OprN efflux system.
  • Biochemical characterization of purified MexT protein's redox properties and oligomerization.

Main Results:

  • Disruption of mexT led to increased susceptibility to diamide, indicating a role in disulfide stress resistance.
  • MexT-regulated targets, such as the MexEF-OprN efflux system, were induced by diamide.
  • Purified MexT formed an oligomeric complex with oxidized glutathione, with a redox potential suggesting it remains reduced under physiological conditions.
  • MexT activation was linked to mutations in mexS, a predicted quinone oxidoreductase, and mexS mutants showed altered cellular redox states.

Conclusions:

  • MexT plays a crucial role in Pseudomonas aeruginosa's intrinsic resistance to disulfide stress.
  • The MexEF-OprN efflux system is implicated in this MexT-mediated resistance.
  • A model is proposed where MexT senses redox signals, potentially via MexS, to activate the MexEF-OprN efflux system for stress resistance.

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