ArticleNature communications2022
CinA mediates multidrug tolerance in Mycobacterium tuberculosis.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 50 citations in OpenAlex.
- Mechanism of the M. tuberculosis DprE1-DprE2 epimerase complex and inhibition by anti-tubercular drugs.Nature chemical biology · 2026Article
- Reactive oxygen detoxification contributes toeLife · 2026Article
- Pretomanid vs delamanid in a bedaquiline-linezolid regimen: efficacy in a high-burden tuberculosis mouse model.Antimicrobial agents and chemotherapy · 2026Article
- Exploiting DprE2 pathway redundancy to enhance potency and overcome resistance to pretomanid in Mycobacterium tuberculosis.npj antimicrobials and resistance · 2026Article
- Metabolic perturbation reduces antibiotic tolerance inMicrobiology (Reading, England) · 2026Article
- Large-scale testing of antimicrobial lethality at single-cell resolution predicts mycobacterial infection outcomes.Nature microbiology · 2026Article
- TheMicrobiology spectrum · 2026Article
- Evaluating selection at intermediate scales within genes provides robust identification of genes under positive selection in M. tuberculosis clinical isolates.Tuberculosis (Edinburgh, Scotland) · 2025Article
- Pyrazinamide killsbioRxiv : the preprint server for biology · 2025Article
- Metabolic rewiring of isoniazid sensitivity inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Reactive Oxygen Detoxification Contributes tobioRxiv : the preprint server for biology · 2025Article
- Evaluating selection at intermediate scales within genes provides robust identification of genes under positive selection inbioRxiv : the preprint server for biology · 2025Article
- A Physiologically Relevant In Vitro Model of Nonreplicating Persistent Mycobacterium tuberculosis in Caseum.Current protocols · 2025Article
- Molecular resistance mechanisms to newly approved antibiotics (2017-2025) in WHO priority pathogens.Frontiers in microbiology · 2025Review
- Association Between Diabetes Mellitus-Tuberculosis and the Generation of Drug Resistance.Microorganisms · 2024Review
- CRISPR Screening and Comparative LC-MS Analysis Identify Genes Mediating Efficacy of Delamanid and Pretomanid against Mycobacterium tuberculosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Drug-resistant tuberculosis: a persistent global health concern.Nature reviews. Microbiology · 2024Review
- Phylogenomic and genomic analysis reveals unique and shared genetic signatures ofMicrobial genomics · 2024Article
- Host stress drives tolerance and persistence: The bane of anti-microbial therapeutics.Cell host & microbe · 2024Review
- A dose-response model for statistical analysis of chemical genetic interactions in CRISPRi screens.PLoS computational biology · 2024Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
The ability of Mycobacterium tuberculosis (Mtb) to resist and tolerate antibiotics complicates the development of improved tuberculosis (TB) chemotherapies. Here we define the Mtb protein CinA as a major determinant of drug tolerance and as a potential target to shorten TB chemotherapy. By reducing the fraction of drug-tolerant persisters, genetic inactivation of cinA accelerated killing of Mtb by four antibiotics in clinical use: isoniazid, ethionamide, delamanid and pretomanid. Mtb ΔcinA was killed rapidly in conditions known to impede the efficacy of isoniazid, such as during nutrient starvation, during persistence in a caseum mimetic, in activated macrophages and during chronic mouse infection. Deletion of CinA also increased in vivo killing of Mtb by BPaL, a combination of pretomanid, bedaquiline and linezolid that is used to treat highly drug-resistant TB. Genetic and drug metabolism studies suggest that CinA mediates drug tolerance via cleavage of NAD-drug adducts.
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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.