ArticlemBio2014
The copper-responsive RicR regulon contributes to Mycobacterium tuberculosis virulence.
Article in mBio, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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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.
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Who cites it
58 citing papers in PubMed, 88 citations in OpenAlex.
- VapC36-mediated intrinsic stress adaption is required for copper tolerance and pathogenesis ofScience advances · 2026Article
- Protein Architecture and Composition in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Review
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- Characterization of a cytokinin-binding protein locus inJournal of bacteriology · 2025Article
- Cu2+ mediates the oxidation of the transcription factor MscA to regulate the antioxidant defense of mycobacteria.Nucleic acids research · 2025Article
- Copper homeostasis; A rapier between mycobacteria and macrophages.FASEB bioAdvances · 2025Review
- Comprehensive whole metagenomics analysis uncovers microbial community and resistome variability across anthropogenically contaminated soils in urban and suburban areas of Tamil Nadu, India.Frontiers in microbiology · 2025Article
- Definition of the effector landscape across 13 phytoplasma proteomes with LEAPH and EffectorComb.NAR genomics and bioinformatics · 2024Article
- The role of transcriptional regulators in metal ion homeostasis ofFrontiers in cellular and infection microbiology · 2024Review
- Copper homeostasis dysregulation in respiratory diseases: a review of current knowledge.Frontiers in physiology · 2024Review
- Mycobacteriaceae Phenome Atlas (MPA): A Standardized Atlas for the Mycobacteriaceae Phenome Based on Heterogeneous Sources.Phenomics (Cham, Switzerland) · 2023Article
- Aldehyde accumulation inmBio · 2023Article
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- Diisonitrile Lipopeptides Mediate Resistance to Copper Starvation in Pathogenic Mycobacteria.mBio · 2022Article
- Mycobacterial resistance to zinc poisoning requires assembly of P-ATPase-containing membrane metal efflux platforms.Nature communications · 2022Article
- Copper microenvironments in the human body define patterns of copper adaptation in pathogenic bacteria.PLoS pathogens · 2022Review
- CtpB FacilitatesInternational journal of molecular sciences · 2022Article
- The aldehyde hypothesis: metabolic intermediates as antimicrobial effectors.Open biology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledAs with most life on Earth, the transition metal copper (Cu) is essential for the viability of the human pathogen Mycobacterium tuberculosis. However, infected hosts can also use Cu to control microbial growth. Several Cu-responsive pathways are present in M. tuberculosis, including the regulated in copper repressor (RicR) regulon, which is unique to pathogenic mycobacteria. In this work, we describe the contribution of each RicR-regulated gene to Cu resistance in vitro and to virulence in animals. We found that the deletion or disruption of individual RicR-regulated genes had no impact on virulence in mice, although several mutants had Cu hypersensitivity. In contrast, a mutant unable to activate the RicR regulon was not only highly susceptible to Cu but also attenuated in mice. Thus, these data suggest that several genes of the RicR regulon are required simultaneously to combat Cu toxicity in vivo or that this regulon is also important for resistance against Cu-independent mechanisms of host defense. IMPORTANCE: Mycobacterium tuberculosis is the causative agent of tuberculosis, killing millions of people every year. Therefore, understanding the biology of M. tuberculosis is crucial for the development of new therapies to treat this devastating disease. Our studies reveal that although host-supplied Cu can suppress bacterial growth, M. tuberculosis has a unique pathway, the RicR regulon, to defend against Cu toxicity. These findings suggest that Cu homeostasis pathways in both the host and the pathogen could be exploited for the treatment of tuberculosis.
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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.