ArticleeLife2024
Cyclic di-GMP as an antitoxin regulates bacterial genome stability and antibiotic persistence in biofilms.
Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed.
- Roles of divalent metals in the regulation of cyclic di-GMP signaling in bacteria.Journal of bacteriology · 2026Review
- Association ofPathogens (Basel, Switzerland) · 2026Article
- Article
- Antibiotic exposure and recovery of persister states influence virulence phenotypes in Pseudomonas aeruginosa.Archives of microbiology · 2026Article
- Antibiotic Persister Cells in Acinetobacter baumannii: Overview of Molecular Mechanisms and Removal Strategies.Environmental microbiology · 2025Review
- RecA Inhibitor Mitigates Bacterial Antibiotic Resistance.Microorganisms · 2025Article
- Bacterial programmed cell death and toxin-antitoxin system in bacteria.Archives of microbiology · 2025Review
- Prokaryotic homeostasis - a solution to thrive and survive.Frontiers in molecular biosciences · 2025Review
- Impact and applications of cyclic di-GMP second messenger signaling in biotechnology and medicine.Sustainable microbiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
Biofilms are complex bacterial communities characterized by a high persister prevalence, which contributes to chronic and relapsing infections. Historically, persister formation in biofilms has been linked to constraints imposed by their dense structures. However, we observed an elevated persister frequency accompanying the stage of cell adhesion, marking the onset of biofilm development. Subsequent mechanistic studies uncovered a comparable type of toxin-antitoxin (TA) module (TA-like system) triggered by cell adhesion, which is responsible for this elevation. In this module, the toxin HipH acts as a genotoxic deoxyribonuclease, inducing DNA double strand breaks and genome instability. While the second messenger c-di-GMP functions as the antitoxin, exerting control over HipH expression and activity. The dynamic interplay between c-di-GMP and HipH levels emerges as a crucial determinant governing genome stability and persister generation within biofilms. These findings unveil a unique TA system, where small molecules act as the antitoxin, outlining a biofilm-specific molecular mechanism influencing genome stability and antibiotic persistence, with potential implications for treating biofilm infections.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.