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Updated: Apr 26, 2026

Population and Single-Cell Analysis of Antibiotic Persistence in Escherichia coli
Published on: March 24, 2023
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.
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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