ArticleAntimicrobial agents and chemotherapy2021
Expression Dysregulation as a Mediator of Fitness Costs in Antibiotic Resistance.
Article in Antimicrobial agents and chemotherapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed.
- Mutations in RNA polymerase that drive the emergence of antibiotic resistance.Current opinion in microbiology · 2026Review
- Transcription attenuation amplifies collateral vulnerabilities in rifampicin-resistant Mycobacterium tuberculosis.Nature microbiology · 2026Article
- Genomic characterization of an extensively drug-resistant Klebsiella pneumoniae co-harboring mcr-3.11, blaNDM-5 and blaCTX-M-27 isolated from pelvic effusion in a colon cancer patient.BMC microbiology · 2026Article
- Key impact of Beijing strains including new resistant clusters on spread of multidrug-resistant tuberculosis in northern Russia.Microbiology spectrum · 2026Article
- LysG-driven transcriptional network rewiring underlies lineage-specific phenotypes in Mycobacterium tuberculosis.Nature communications · 2026Article
- Eco-evolutionary dynamics and environmental detoxification jointly shape bacterial community response to antibiotic perturbation.The ISME journal · 2026Article
- Extensive Endemic Transmission of Multidrug-ResistantOpen forum infectious diseases · 2026Article
- Unraveling Epistatic Interactions Between Sites Under Drug-Dependent Selection in the Mycobacterium tuberculosis Genome.Molecular biology and evolution · 2025Article
- Deciphering the Impact of Temperature on Pleiotropic Consequences of RNA Polymerase Mutations.Molecular biology and evolution · 2025Article
- Large-scale statistical analysis of Mycobacterium tuberculosis genome sequences identifies compensatory mutations associated with multi-drug resistance.Scientific reports · 2024Article
- Long-Term Co-Circulation of Host-Specialist and Host-Generalist Lineages of Group BAntibiotics (Basel, Switzerland) · 2024Article
- Article
- Pervasive genotype-by-environment interactions shape the fitness effects of antibiotic resistance mutations.Proceedings. Biological sciences · 2023Article
- The relative transmission fitness of multidrug-resistant Mycobacterium tuberculosis in a drug resistance hotspot.Nature communications · 2023Article
- Evolution ofFrontiers in cellular and infection microbiology · 2022Review
- Dissecting the Fitness Costs of Complex Mutations.Molecular biology and evolution · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Antimicrobial resistance (AMR) poses a threat to global health and the economy. Rifampicin-resistant Mycobacterium tuberculosis accounts for a third of the global AMR burden. Gaining the upper hand on AMR requires a deeper understanding of the physiology of resistance. AMR often results in a fitness cost in the absence of drug. Identifying the molecular mechanisms underpinning this cost could help strengthen future treatment regimens. Here, we used a collection of M. tuberculosis strains that provide an evolutionary and phylogenetic snapshot of rifampicin resistance and subjected them to genome-wide transcriptomic and proteomic profiling to identify key perturbations of normal physiology. We found that the clinically most common rifampicin resistance-conferring mutation, RpoB Ser450Leu, imparts considerable gene expression changes, many of which are mitigated by the compensatory mutation in RpoC Leu516Pro. However, our data also provide evidence for pervasive epistasis-the same resistance mutation imposed a different fitness cost and functionally distinct changes to gene expression in genetically unrelated clinical strains. Finally, we report a likely posttranscriptional modulation of gene expression that is shared in most of the tested strains carrying RpoB Ser450Leu, resulting in an increased abundance of proteins involved in central carbon metabolism. These changes contribute to a more general trend in which the disruption of the composition of the proteome correlates with the fitness cost of the RpoB Ser450Leu mutation in different strains.
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.