ArticleScientific reports2017
Co-expression network analysis of toxin-antitoxin loci in Mycobacterium tuberculosis reveals key modulators of cellular stress.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 54 papers, 1 of them a synthesis that pooled it.
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- Meta-analysis Reveals Potential Influence of Oxidative Stress on the Airway Microbiomes of Cystic Fibrosis Patients.Genomics, proteomics & bioinformatics · 2019Pooled it
- Structural and functional characterization of VapBC52 toxin-antitoxin system from Mycobacterium tuberculosis.Nucleic acids research · 2026Article
- VapC36-mediated intrinsic stress adaption is required for copper tolerance and pathogenesis ofScience advances · 2026Article
- Hardwired survival algorithms: RelBE1 and MadR1 couple carbon state to metabolic persistence inFrontiers in microbiology · 2026Article
- Ser/Thr phosphorylation ofmBio · 2025Article
- The identification Mycobacterium tuberculosis genes that modulate long term survival in the presence of rifampicin and streptomycin.Scientific reports · 2025Article
- Effect of Pefloxacin onAntibiotics (Basel, Switzerland) · 2025Article
- Understanding the physiological role and cross-interaction network of VapBC35 toxin-antitoxin system from Mycobacterium tuberculosis.Communications biology · 2025Article
- Insight into the environmental cues modulating the expression of bacterial toxin-antitoxin systems.FEMS microbiology reviews · 2025Review
- Preliminary transcriptomic analyses revealFrontiers in microbiology · 2025Article
- Comprehensive pan-genome analysis of Mycobacterium marinum: insights into genomic diversity, evolution, and pathogenicity.Scientific reports · 2024Article
- Toxin-mediated depletion of NAD and NADP drives persister formation in a human pathogen.The EMBO journal · 2024Article
- Deciphering the role of VapBC13 and VapBC26 toxin antitoxin systems in the pathophysiology of Mycobacterium tuberculosis.Communications biology · 2024Article
- Mycobacterium tuberculosis strain with deletions in menT3 and menT4 is attenuated and confers protection in mice and guinea pigs.Nature communications · 2024Article
- HigA2 (Rv2021c) Is a Transcriptional Regulator with Multiple Regulatory Targets inMicroorganisms · 2024Article
- Gene Regulatory Mechanism of Mycobacterium Tuberculosis during Dormancy.Current issues in molecular biology · 2024Review
- Toxin release by conditional remodelling of ParDE1 from Mycobacterium tuberculosis leads to gyrase inhibition.Nucleic acids research · 2024Article
- Are all VapC toxins ofJournal of biosciences · 2024Article
- Revolutionizing control strategies against Mycobacterium tuberculosis infection through selected targeting of lipid metabolism.Cellular and molecular life sciences : CMLS · 2023Review
- Bacterial Toxin-Antitoxin Systems' Cross-Interactions-Implications for Practical Use in Medicine and Biotechnology.Toxins · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Research on toxin-antitoxin loci (TA loci) is gaining impetus due to their ubiquitous presence in bacterial genomes and their observed roles in stress survival, persistence and drug tolerance. The present study investigates the expression profile of all the seventy-nine TA loci found in Mycobacterium tuberculosis. The bacterium was subjected to multiple stress conditions to identify key players of cellular stress response and elucidate a TA-coexpression network. This study provides direct experimental evidence for transcriptional activation of each of the seventy-nine TA loci following mycobacterial exposure to growth-limiting environments clearly establishing TA loci as stress-responsive modules in M. tuberculosis. TA locus activation was found to be stress-specific with multiple loci activated in a duration-based response to a particular stress. Conditions resulting in arrest of cellular translation led to greater up-regulation of TA genes suggesting that TA loci have a primary role in arresting translation in the cell. Our study identifed higBA2 and vapBC46 as key loci that were activated in all the conditions tested. Besides, relBE1, higBA3, vapBC35, vapBC22 and higBA1 were also upregulated in multpile stresses. Certain TA modules exhibited co-activation across multiple conditions suggestive of a common regulatory mechanism.
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