ArticleBMC microbiology2013
MazF6 toxin of Mycobacterium tuberculosis demonstrates antitoxin specificity and is coupled to regulation of cell growth by a Soj-like protein.
Article in BMC microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 26 citations in OpenAlex.
- Hardwired survival algorithms: RelBE1 and MadR1 couple carbon state to metabolic persistence inFrontiers in microbiology · 2026Article
- The identification Mycobacterium tuberculosis genes that modulate long term survival in the presence of rifampicin and streptomycin.Scientific reports · 2025Article
- Long Dynamic β1-β2 Loops inInternational journal of molecular sciences · 2024Article
- Identification of Genes Encoded Toxin-Antitoxin System inInfectious disorders drug targets · 2024Article
- Tale of Twin Bifunctional Second Messenger (p)ppGpp Synthetases and Their Function in Mycobacteria.ACS omega · 2023Review
- Septum site placement inMicrobiology (Reading, England) · 2023Article
- A tRNA-Acetylating Toxin and Detoxifying Enzyme in Mycobacterium tuberculosis.Microbiology spectrum · 2022Article
- Discovery of a novel type IIb RelBE toxin-antitoxin system in Mycobacterium tuberculosis defined by co-regulation with an antisense RNA.Molecular microbiology · 2022Article
- Clinically encountered growth phenotypes of tuberculosis-causing bacilli and theirFrontiers in cellular and infection microbiology · 2022Review
- Rapid Identification of Secondary Structure and Binding Site Residues in an Intrinsically Disordered Protein Segment.Frontiers in genetics · 2021Article
- HigB1 Toxin inFrontiers in microbiology · 2021Article
- Review
- Article
- DivIVA Controls Progeny Morphology and Diverse ParA Proteins Regulate Cell Division or Gliding Motility inFrontiers in microbiology · 2020Article
- Emerging Roles of Toxin-Antitoxin Modules in Bacterial Pathogenesis.Molecules (Basel, Switzerland) · 2016Review
- tRNA is a new target for cleavage by a MazF toxin.Nucleic acids research · 2016Article
- MadR1, a Mycobacterium tuberculosis cell cycle stress response protein that is a member of a widely conserved protein class of prokaryotic, eukaryotic and archeal origin.Tuberculosis (Edinburgh, Scotland) · 2015Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundMolecular programs employed by Mycobacterium tuberculosis (Mtb) for the establishment of non-replicating persistence (NRP) are poorly understood. In order to investigate mechanisms regulating entry into NRP, we asked how cell cycle regulation is linked to downstream adaptations that ultimately result in NRP. Based on previous reports and our recent studies, we reason that, in order to establish NRP, cells are halted in the cell cycle at the point of septum formation by coupled regulatory mechanisms.
resultsUsing bioinformatic consensus modeling, we identified an alternative cell cycle regulatory element, Soj(Mtb) encoded by rv1708. Soj(Mtb) coordinates a regulatory mechanism involving cell cycle control at the point of septum formation and elicits the induction of the MazF6 toxin. MazF6 functions as an mRNA interferase leading to bacteriostasis that can be prevented by interaction with its cognate antitoxin, MazE6. Further, MazEF6 acts independently of other Maz family toxin:antitoxin pairs. Notably, soj(Mtb) and mazEF6 transcripts where identified at 20, 40 and 100 days post-infection in increasing abundance indicating a role in adaption during chronic infection.
conclusionsHere we present the first evidence of a coupled regulatory system in which cell cycle regulation via Soj(Mtb) is linked to downstream adaptations that are facilitated through the activity of the MazEF6 TA pair.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.