ArticleMolecular microbiology2014
Fitness costs of rifampicin resistance in Mycobacterium tuberculosis are amplified under conditions of nutrient starvation and compensated by mutation in the β' subunit of RNA polymerase.
Article in Molecular microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed.
- Transcription attenuation amplifies collateral vulnerabilities in rifampicin-resistant Mycobacterium tuberculosis.Nature microbiology · 2026Article
- Exploring transmission dynamics in epidemiologically linked pulmonary tuberculosis cases and household contacts: a WGS-based investigation.BMC genomics · 2025Article
- Genomic characterization and epidemiology of Mycobacterium tuberculosis lineage 2 isolates from Kazakhstan.Scientific reports · 2025Article
- Deciphering the Impact of Temperature on Pleiotropic Consequences of RNA Polymerase Mutations.Molecular biology and evolution · 2025Article
- Subpopulations in clinical samples ofJAC-antimicrobial resistance · 2025Article
- Fragment-Based Development of Small Molecule Inhibitors TargetingJournal of medicinal chemistry · 2025Article
- The Risk Factors Associated with the Carriage to Critical Antimicrobial-ResistantAnimals : an open access journal from MDPI · 2025Article
- The yin and yang of the universal transcription factor NusG.Current opinion in microbiology · 2024Review
- Reassessment of the genetic basis of natural rifampin resistance in the genus Rickettsia.MicrobiologyOpen · 2024Article
- Prevalence of antibiotic-resistantFood science and biotechnology · 2024Article
- Large-scale statistical analysis of Mycobacterium tuberculosis genome sequences identifies compensatory mutations associated with multi-drug resistance.Scientific reports · 2024Article
- Grow now, pay later: When should a bacterium go into debt?Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- Compensatory mutations are associated with increasedMicrobial genomics · 2024Article
- Multidrug-resistant tuberculosis clusters and transmission in Taiwan: a population-based cohort study.Frontiers in microbiology · 2024Article
- Genetic diversity, evolution and drug resistance ofFrontiers in microbiology · 2024Review
- Genomic Characterization of Drug-ResistantAntibiotics (Basel, Switzerland) · 2023Article
- Pervasive genotype-by-environment interactions shape the fitness effects of antibiotic resistance mutations.Proceedings. Biological sciences · 2023Article
- Molecular Analysis of Anti-Tuberculosis Drug Resistance ofAntibiotics (Basel, Switzerland) · 2023Article
- The relative transmission fitness of multidrug-resistant Mycobacterium tuberculosis in a drug resistance hotspot.Nature communications · 2023Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
22 authors.
Funding
Abstract
Rifampicin resistance, a defining attribute of multidrug-resistant tuberculosis, is conferred by mutations in the β subunit of RNA polymerase. Sequencing of rifampicin-resistant (RIF-R) clinical isolates of Mycobacterium tuberculosis revealed, in addition to RIF-R mutations, enrichment of potential compensatory mutations around the double-psi β-barrel domain of the β' subunit comprising the catalytic site and the exit tunnel for newly synthesized RNA. Sequential introduction of the resistance allele followed by the compensatory allele in isogenic Mycobacterium smegmatis showed that these mutations respectively caused and compensated a starvation enhanced growth defect by altering RNA polymerase activity. While specific combinations of resistance and compensatory alleles converged in divergent lineages, other combinations recurred among related isolates suggesting transmission of compensated RIF-R strains. These findings suggest nutrient poor growth conditions impose larger selective pressure on RIF-R organisms that results in the selection of compensatory mutations in a domain involved in catalysis and starvation control of RNA polymerase transcription.
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.