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A Salmonella Toxin Promotes Persister Formation through Acetylation of tRNA

Angela M Cheverton1, Bridget Gollan1, Michal Przydacz2

  • 1Section of Microbiology, Medical Research Council Centre for Molecular Bacteriology and Infection, Imperial College London, London SW7 2AZ, UK.

Molecular Cell
|June 7, 2016
PubMed

Insights

Bacterial persisters, antibiotic-tolerant cells, form via toxin TacT inhibiting translation. Peptidyl-tRNA hydrolase counteracts TacT, enabling persister growth and explaining infection relapse.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Structural Biology

Background:

  • Bacterial infections often resist antibiotics due to persister cells, which are dormant and insensitive to drugs.
  • Salmonella's survival within macrophages involves forming persisters through toxin-antitoxin systems.
  • Understanding persister formation and resuscitation is crucial for treating persistent infections.

Purpose of the Study:

  • To elucidate the mechanism by which the toxin TacT induces persister formation in Salmonella.
  • To determine the structural basis of TacT toxicity.
  • To identify mechanisms that allow persister cells to resume growth.

Main Methods:

  • Biochemical assays to characterize TacT activity as an acetyltransferase.
  • X-ray crystallography to determine the structure of TacT.
  • Genetic and biochemical experiments to investigate the interaction between TacT and peptidyl-tRNA hydrolase.

Main Results:

  • TacT acts as an acetyltransferase, modifying charged tRNA to inhibit translation and promote persister formation.
  • The crystal structure of TacT reveals unique positively charged surface patches critical for its toxic function.
  • Peptidyl-tRNA hydrolase was identified as a counteracting enzyme that reverses TacT's effects, allowing growth resumption.

Conclusions:

  • TacT-mediated tRNA acetylation is a key mechanism for Salmonella persister formation.
  • The structural insights into TacT provide a basis for understanding its function and potential inhibition.
  • The discovery of peptidyl-tRNA hydrolase as a detoxifying agent explains persister resuscitation and offers targets for therapeutic intervention.

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