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Toxin YafQ increases persister cell formation by reducing indole signalling

Ying Hu1, Brian W Kwan, Devon O Osbourne

  • 1Department of Chemical Engineering and, Pennsylvania State University, University Park, PA, 16802-4400, USA.

Environmental Microbiology
|July 22, 2014
PubMed

Insights

Toxin YafQ from Escherichia coli toxin/antitoxin systems increases persister cell formation by cleaving specific mRNA transcripts. This toxin reduces indole levels, a key factor in bacterial stress survival.

Area of Science:

  • Microbiology
  • Bacterial Physiology
  • Molecular Biology

Background:

  • Persister cells are crucial for bacterial survival under antibiotic stress by entering a dormant state.
  • Toxin/antitoxin (TA) systems are implicated in persister cell formation, but the exact mechanisms are not fully understood.

Purpose of the Study:

  • To investigate the role of YafQ, a toxin from the YafQ/DinJ TA system in Escherichia coli, in persister cell formation.
  • To elucidate the molecular mechanisms by which YafQ influences bacterial stress resistance.

Main Methods:

  • Assessing persister cell formation in the presence of YafQ under various antibiotic stresses.
  • Analyzing changes in protein and mRNA expression, specifically targeting tryptophanase (TnaA) and RpoS.
  • Measuring indole levels and evaluating the impact of indole manipulation on persistence.

Main Results:

  • YafQ production significantly increased persister cell formation across multiple antibiotics.
  • YafQ reduced tryptophanase (TnaA) and stationary-phase sigma factor RpoS levels by cleaving their respective mRNAs.
  • Reduced indole production, a downstream effect of YafQ activity, was directly correlated with increased persistence.

Conclusions:

  • YafQ enhances bacterial persistence by downregulating indole synthesis through TnaA and RpoS.
  • This study highlights a novel link between TA systems, metabolic regulation, and bacterial stress survival.
  • YafQ's mechanism provides insights into bacterial cell signaling and antibiotic resistance strategies.

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