ArticlePloS one2012
The ζ toxin induces a set of protective responses and dormancy.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Enhancement of Menaquinone-7 production in Bacillus subtilis by optimizing the medium components through response surface methodology.Bioresources and bioprocessing · 2025Article
- Type II bacterial toxin-antitoxins: hypotheses, facts, and the newfound plethora of the PezAT system.FEMS microbiology reviews · 2023Article
- Bacterial toxin-antitoxin systems: Novel insights on toxin activation across populations and experimental shortcomings.Current research in microbial sciences · 2023Review
- An Auto-Regulating Type II Toxin-Antitoxin System Modulates Drug Resistance and Virulence inFrontiers in microbiology · 2021Article
- Article
- Article
- Toxin ζ Reduces the ATP and Modulates the Uridine Diphosphate-N-acetylglucosamine Pool.Toxins · 2019Article
- TheToxins · 2018Article
- Commentary: What Is the Link between Stringent Response, Endoribonuclease Encoding Type II Toxin-Antitoxin Systems and Persistence?Frontiers in microbiology · 2017Article
- Toxin ζ Triggers a Survival Response to Cope with Stress and Persistence.Frontiers in microbiology · 2017Article
- Article
- Keeping the Wolves at Bay: Antitoxins of Prokaryotic Type II Toxin-Antitoxin Systems.Frontiers in molecular biosciences · 2016Review
- The interaction of ω2 with the RNA polymerase β' subunit functions as an activation to repression switch.Nucleic acids research · 2015Article
- Bacillus subtilis RecO and SsbA are crucial for RecA-mediated recombinational DNA repair.Nucleic acids research · 2015Article
- Roles of Bacillus subtilis DprA and SsbA in RecA-mediated genetic recombination.The Journal of biological chemistry · 2014Article
- Article
- The presence of conjugative plasmid pLS20 affects global transcription of Its Bacillus subtilis host and confers beneficial stress resistance to cells.Applied and environmental microbiology · 2014Article
- VapC from the leptospiral VapBC toxin-antitoxin module displays ribonuclease activity on the initiator tRNA.PloS one · 2014Article
- Article
- To be or not to be: regulation of restriction-modification systems and other toxin-antitoxin systems.Nucleic acids research · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ζε module consists of a labile antitoxin protein, ε, which in dimer form (ε(2)) interferes with the action of the long-living monomeric ζ phosphotransferase toxin through protein complex formation. Toxin ζ, which inhibits cell wall biosynthesis and may be bactericide in nature, at or near physiological concentrations induces reversible cessation of Bacillus subtilis proliferation (protective dormancy) by targeting essential metabolic functions followed by propidium iodide (PI) staining in a fraction (20-30%) of the population and selects a subpopulation of cells that exhibit non-inheritable tolerance (1-5×10(-5)). Early after induction ζ toxin alters the expression of ∼78 genes, with the up-regulation of relA among them. RelA contributes to enforce toxin-induced dormancy. At later times, free active ζ decreases synthesis of macromolecules and releases intracellular K(+). We propose that ζ toxin induces reversible protective dormancy and permeation to PI, and expression of ε(2) antitoxin reverses these effects. At later times, toxin expression is followed by death of a small fraction (∼10%) of PI stained cells that exited earlier or did not enter into the dormant state. Recovery from stress leads to de novo synthesis of ε(2) antitoxin, which blocks ATP binding by ζ toxin, thereby inhibiting its phosphotransferase activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.