ArticleThe Journal of biological chemistry2010
Mycobacterium tuberculosis origin of replication and the promoter for immunodominant secreted antigen 85B are the targets of MtrA, the essential response regulator.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed.
- Exploring the Protein Landscape of Dormant Mycobacterium tuberculosis Through In Vitro Functional Studies.Advances in experimental medicine and biology · 2026Review
- Crosstalk between cyclic-di-guanosine monophosphate and the sensor kinase MtrB regulates MtrA-dependent genes, bacterial growth, biofilm formation and lysosomal trafficking ofMicrobiology (Reading, England) · 2025Article
- Structure-guided identification and characterization of potent inhibitors targeting PhoP and MtrA to combat mycobacteria.Computational and structural biotechnology journal · 2024Article
- Regulatory role ofFrontiers in microbiology · 2024Article
- Substrate DNA Promoting Binding ofMicroorganisms · 2023Article
- MtrA modulates Mycobacterium tuberculosis cell division in host microenvironments to mediate intrinsic resistance and drug tolerance.Cell reports · 2023Article
- Mutation of MtrA at the Predicted Phosphorylation Site Abrogates Its Role as a Global Regulator in Streptomyces venezuelae.Microbiology spectrum · 2022Article
- Article
- Recent Advances in Histidine Kinase-Targeted Antimicrobial Agents.Frontiers in chemistry · 2022Review
- Article
- 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
- Reference genome and comparative genome analysis for the WHO reference strain for Mycobacterium bovis BCG Danish, the present tuberculosis vaccine.BMC genomics · 2019Article
- Changing Perspectives on the Role of DnaA-ATP in Orisome Function and Timing Regulation.Frontiers in microbiology · 2019Review
- The NnaR orphan response regulator is essential for the utilization of nitrate and nitrite as sole nitrogen sources in mycobacteria.Scientific reports · 2018Article
- Multisystem Analysis ofmBio · 2018Article
- 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
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Efficient proliferation of Mycobacterium tuberculosis (Mtb) inside macrophage requires that the essential response regulator MtrA be optimally phosphorylated. However, the genomic targets of MtrA have not been identified. We show by chromatin immunoprecipitation and DNase I footprinting that the chromosomal origin of replication, oriC, and the promoter for the major secreted immunodominant antigen Ag85B, encoded by fbpB, are MtrA targets. DNase I footprinting analysis revealed that MtrA recognizes two direct repeats of GTCACAgcg-like sequences and that MtrA approximately P, the phosphorylated form of MtrA, binds preferentially to these targets. The oriC contains several MtrA motifs, and replacement of all motifs or of a single select motif with TATATA compromises the ability of oriC plasmids to maintain stable autonomous replication in wild type and MtrA-overproducing strains, indicating that the integrity of the MtrA motif is necessary for oriC replication. The expression of the fbpB gene is found to be down-regulated in Mtb cells upon infection when these cells overproduce wild type MtrA but not when they overproduce a nonphosphorylated MtrA, indicating that MtrA approximately P regulates fbpB expression. We propose that MtrA is a regulator of oriC replication and that the ability of MtrA to affect apparently unrelated targets, i.e. oriC and fbpB, reflects its main role as a coordinator between the proliferative and pathogenic functions of Mtb.
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