ArticleScientific reports2025
Escherichia coli type I toxin TisB exclusively controls proton depolarization following antibiotic induced DNA damage.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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Who cites it
4 citing papers in PubMed.
- Antimicrobial Peptides Based on the TisB Toxin: Toward Enhanced Activity and Synergy with Antibiotics.ACS omega · 2026Article
- Spontaneous TisB toxin expression modulatesFEMS microbes · 2026Article
- The Prevalence and Diversity of Marine Toxin-Antitoxin Systems.Marine drugs · 2025Article
- Functional diversity and molecular interactions of small membrane proteins in bacteria.microLife · 2025Review
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Authors and funding
5 authors.
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Abstract
Bacterial toxin-antitoxin (TA) systems are genetic loci where the antitoxin gene product helps to control the expression or activity of the toxin gene product. Type I TA systems typically produce hydrophobic peptides that often localize to the inner membrane of bacteria. These amphipathic peptides can then potentially affect ion flows across the inner membrane. Here, we show that several type I toxins from Escherichia coli can affect depolarization, whereas tisB exclusively controls the depolarization of the proton gradient. tisB has been linked to persister cell formation following treatment with the antibiotic ciprofloxacin and tisB-istR has been implicated in the control of proton depolarization following treatment with ofloxacin. These results suggest that tisB could initiate the formation of persister cells by fully dissipating the proton gradient and that most of the electrical gradient greatly limiting ATP production following antibiotic-induced DNA damage.
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