ArticlePLoS pathogens2007
Mycobacterium tuberculosis nuoG is a virulence gene that inhibits apoptosis of infected host cells.
Article in PLoS pathogens, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 179 papers.
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Who cites it
179 citing papers in PubMed, 321 citations in OpenAlex.
- Organelle interplay in host responses and mycobacterial resilience.EMBO reports · 2026Review
- Mitochondrial STAT3-mediated suppression of apoptosis constrains antimycobacterial immunity.bioRxiv : the preprint server for biology · 2026Article
- Characterization of programmed cell death pathways activated in Mycobacterium tuberculosis-infected human macrophages.Cell death discovery · 2026Article
- High-throughput characterization of Mycobacterium tuberculosis gene function across diverse conditions.PLoS biology · 2026Article
- Protein-Mediated Virulence in Mycobacterium tuberculosis.Advances in experimental medicine and biology · 2026Review
- Respiratory chain gene mutations associated with global phylogenetic clustering of drug-resistantFrontiers in immunology · 2026Article
- CDK1‑induced regulation of p53 phosphorylation at Ser315 mediates cell cycle arrest and apoptosis of macrophages infected with clinical isolates ofMolecular medicine reports · 2026Article
- Discerning dangerous gain of function: most gain of function (GoF) research does not involve infectious microbes.Frontiers in bioengineering and biotechnology · 2026Review
- Research progress in PANoptosis mechanisms and their interplay with tuberculosis.Frontiers in cellular and infection microbiology · 2026Review
- Finding and filling the knowledge gaps in mechanisms of T cell-mediated TB immunity to inform vaccine design.Nature reviews. Immunology · 2025Review
- Cell death pathways in response toInfection and immunity · 2025Review
- How macrophage heterogeneity affects tuberculosis disease and therapy.Nature reviews. Immunology · 2025Review
- Repurposing of apoptotic inducer drugs against Mycobacterium tuberculosis.Scientific reports · 2025Article
- Iron-restricted Mycobacterium tuberculosis exports pathogenicity factors packed in extracellular vesicles.PloS one · 2025Article
- Epigenetic Mechanisms Induced byInternational journal of molecular sciences · 2024Review
- Association of mutations in Mycobacterium tuberculosis complex (MTBC) respiration chain genes with hyper-transmission.BMC genomics · 2024Article
- Live Attenuated Vaccines against Tuberculosis: Targeting the Disruption of Genes Encoding the Secretory Proteins of Mycobacteria.Vaccines · 2024Review
- Lsr2, a pleiotropic regulator at the core of the infectious strategy ofMicrobiology spectrum · 2024Article
- CpsA mediates infection of recruited lung myeloid cells by Mycobacterium tuberculosis.Cell reports · 2024Article
- From pathogenesis to antigens: the key to shaping the future of TB vaccines.Frontiers in immunology · 2024Review
119 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
10 authors at 3 institutions in 1 country.
Funding
Abstract
The survival and persistence of Mycobacterium tuberculosis depends on its capacity to manipulate multiple host defense pathways, including the ability to actively inhibit the death by apoptosis of infected host cells. The genetic basis for this anti-apoptotic activity and its implication for mycobacterial virulence have not been demonstrated or elucidated. Using a novel gain-of-function genetic screen, we demonstrated that inhibition of infection-induced apoptosis of macrophages is controlled by multiple genetic loci in M. tuberculosis. Characterization of one of these loci in detail revealed that the anti-apoptosis activity was attributable to the type I NADH-dehydrogenase of M. tuberculosis, and was mainly due to the subunit of this multicomponent complex encoded by the nuoG gene. Expression of M. tuberculosis nuoG in nonpathogenic mycobacteria endowed them with the ability to inhibit apoptosis of infected human or mouse macrophages, and increased their virulence in a SCID mouse model. Conversely, deletion of nuoG in M. tuberculosis ablated its ability to inhibit macrophage apoptosis and significantly reduced its virulence in mice. These results identify a key component of the genetic basis for an important virulence trait of M. tuberculosis and support a direct causal relationship between virulence of pathogenic mycobacteria and their ability to inhibit macrophage apoptosis.
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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.