ArticleMolecular microbiology2015
Mycobacterium tuberculosis oriC sequestration by MtrA response regulator.
Article in Molecular microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed.
- Robust helicase loading mechanism underlies diverse architectures of bacterial replication origins.Nucleic acids research · 2026Article
- MtrAB activates ectoine production and triggers sporulation in response to osmotic stress inMicrobiology (Reading, England) · 2026Article
- Characterization of a pleiotropic regulator MtrA in Streptomyces avermitilis controlling avermectin production and morphological differentiation.Microbial cell factories · 2024Article
- Substrate DNA Promoting Binding ofMicroorganisms · 2023Article
- The Bacterial MtrAB Two-Component System Regulates the Cell Wall Homeostasis Responding to Environmental Alkaline Stress.Microbiology spectrum · 2022Article
- The Roles of the Two-Component System, MtrAB, in Response to Diverse Cell Envelope Stresses inApplied and environmental microbiology · 2022Article
- Mutation of MtrA at the Predicted Phosphorylation Site Abrogates Its Role as a Global Regulator in Streptomyces venezuelae.Microbiology spectrum · 2022Article
- Article
- Contribution of NmSystems · 2021Article
- HP1021 is a redox switch protein identified in Helicobacter pylori.Nucleic acids research · 2021Article
- Methylation of two-component response regulator MtrA in mycobacteria negatively modulates its DNA binding and transcriptional activation.The Biochemical journal · 2020Article
- Impact on Multiple Antibiotic Pathways Reveals MtrA as a Master Regulator of Antibiotic Production inApplied and environmental microbiology · 2020Article
- Protein kinases PknA and PknB independently and coordinately regulate essential Mycobacterium tuberculosis physiologies and antimicrobial susceptibility.PLoS pathogens · 2020Article
- Acetylation of Response Regulator Protein MtrA inFrontiers in microbiology · 2020Article
- Blocking the Trigger: Inhibition of the Initiation of Bacterial Chromosome Replication as an Antimicrobial Strategy.Antibiotics (Basel, Switzerland) · 2019Review
- Dissolution of the Disparate: Co-ordinate Regulation in Antibiotic Biosynthesis.Antibiotics (Basel, Switzerland) · 2019Review
- NapM enhances the survival ofCommunications biology · 2019Article
- Essential Two-Component Systems Regulating Cell Envelope Functions: Opportunities for Novel Antibiotic Therapies.The Journal of membrane biology · 2018Review
- MtrA Response Regulator Controls Cell Division and Cell Wall Metabolism and Affects Susceptibility of Mycobacteria to the First Line Antituberculosis Drugs.Frontiers in microbiology · 2018Article
- Structure and Function of theFrontiers in microbiology · 2018Article
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.
Funding
Abstract
The regulators of Mycobacterium tuberculosis DNA replication are largely unknown. Here, we demonstrate that in synchronously replicating M. tuberculosis, MtrA access to origin of replication (oriC) is enriched in the post-replication (D) period. The increased oriC binding results from elevated MtrA phosphorylation (MtrA∼P) as evidenced by reduced expression of dnaN, dnaA and increased expression of select cell division targets. Overproduction of gain-of-function MtrAY102C advanced the MtrA oriC access to the C period, reduced dnaA and dnaN expression, interfered with replication synchrony and compromised cell division. Overproduction of wild-type (MtrA+) or phosphorylation-defective MtrAD56N did not promote oriC access in the C period, nor affected cell cycle progression. MtrA interacts with DnaA signaling a possibility that DnaA helps load MtrA on oriC. Therefore, oriC sequestration by MtrA∼P in the D period may normally serve to prevent untimely initiations and that DnaA-MtrA interactions may facilitate regulated oriC replication. Finally, despite the near sequence identity of MtrA in M. smegmatis and M. tuberculosis, the M. smegmatis oriC is not MtrA-target. We conclude that M. tuberculosis oriC has evolved to be regulated by MtrA and that cell cycle progression in this organisms are governed, at least in part, by oscillations in the MtrA∼P levels.
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.