ArticleNature microbiology2018
Clinically prevalent mutations in Mycobacterium tuberculosis alter propionate metabolism and mediate multidrug tolerance.
Article in Nature microbiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 1 of them a synthesis that pooled it.
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Who cites it
131 citing papers in PubMed, 1 synthesis or guideline pooled it, 252 citations in OpenAlex.
- In Host Mutational Adaptation of Mycobacterium Tuberculosis Complex Strains During Tuberculosis Infection.The Journal of infectious diseases · 2026Pooled it
- Variation in multiple classes of simple sequence repeats can alter drug susceptibility inbioRxiv : the preprint server for biology · 2026Article
- Article
- Heterogeneity in microbial antibiotic responses: genetic basis and within-host evolution.Trends in genetics : TIG · 2026Review
- Article
- Within-host pathogen population diversity predicts treatment response in Tuberculosis.medRxiv : the preprint server for health sciences · 2026Article
- A versatile multi-components mixed model for bacterial-Genome Wide association studies.Nature communications · 2026Article
- Ribosomal RNA methylation by GidB modulates discrimination of mischarged tRNA.bioRxiv : the preprint server for biology · 2026Article
- Dormancy regulon reduction was pivotal to the evolution of Mycobacterium tuberculosis.Nature communications · 2026Article
- Metabolic perturbation reduces antibiotic tolerance inMicrobiology (Reading, England) · 2026Article
- Mycobacterium tuberculosis MutT4/RppH is an RNA pyrophosphohydrolase that forms condensate-like bodies and impacts mRNA degradation.Nucleic acids research · 2026Article
- Profiling of BDQ-induced transcriptome suggests amino acid metabolism and stress responses as alternate mechanisms contributing to BDQ tolerance inMicrobiology spectrum · 2026Article
- Large-scale testing of antimicrobial lethality at single-cell resolution predicts mycobacterial infection outcomes.Nature microbiology · 2026Article
- Mutations in sugar metabolism-related genes driving global drug-resistant Mycobacterium tuberculosis transmission revealed by whole-genome sequencing.BMC infectious diseases · 2026Article
- Article
- Respiratory chain gene mutations associated with global phylogenetic clustering of drug-resistantFrontiers in immunology · 2026Article
- Current drug susceptibility testing in the Löwenstein-Jensen medium leads to underestimating of prothionamide resistance in multi-drug resistant Mycobacterium tuberculosis.BMC microbiology · 2025Article
- Variability in intrinsic drug tolerance inAntimicrobial agents and chemotherapy · 2025Article
- Evaluating selection at intermediate scales within genes provides robust identification of genes under positive selection in M. tuberculosis clinical isolates.Tuberculosis (Edinburgh, Scotland) · 2025Article
- Article
71 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
Abstract
The global epidemic of drug-resistant tuberculosis is a catastrophic example of how antimicrobial resistance is undermining the public health gains made possible by combination drug therapy. Recent evidence points to unappreciated bacterial factors that accelerate the emergence of drug resistance. In a genome-wide association study of Mycobacterium tuberculosis isolates from China, we find mutations in the gene encoding the transcription factor prpR enriched in drug-resistant strains. prpR mutations confer conditional drug tolerance to three of the most effective classes of antibiotics by altering propionyl-CoA metabolism. prpR-mediated drug tolerance is carbon-source dependent, and while readily detectable during infection of human macrophages, is not captured by standard susceptibility testing. These data define a previously unrecognized and clinically prevalent class of M. tuberculosis variants that undermine antibiotic efficacy and drive drug resistance.
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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.