ArticleMolecular microbiology2013
A novel F(420) -dependent anti-oxidant mechanism protects Mycobacterium tuberculosis against oxidative stress and bactericidal agents.
Article in Molecular microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 124 citations in OpenAlex.
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- Flavin and deazaflavin biosynthesis in mycobacteria: relevance to physiology, implications for drug discovery, MR-1 antigenicity, and vaccine development.Frontiers in immunology · 2025Review
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- Using Mycobacterium smegmatis as a Bioindicator for Zinc-limited Growth Conditions in Mycobacteria.Journal of visualized experiments : JoVE · 2024Article
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- Harnessing redox proteomics to study metabolic regulation and stress response in lignin-fed Rhodococci.Biotechnology for biofuels and bioproducts · 2023Article
- Genomics of soil depth niche partitioning in the Thaumarchaeota family Gagatemarchaeaceae.Nature communications · 2023Article
- Production of copropophyrin III, biliverdin and bilirubin by the rufomycin producer,Frontiers in microbiology · 2023Article
- Metabolic tuning of a stable microbial community in the surface oligotrophic Indian Ocean revealed by integrated meta-omics.Marine life science & technology · 2022Article
- Diversification by CofC and Control by CofD Govern Biosynthesis and Evolution of Coenzyme FmBio · 2022Article
- Transcriptional regulation and drug resistance inFrontiers in cellular and infection microbiology · 2022Review
2 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Mycobacterium tuberculosis (Mtb) is an aerobic bacterium that persists intracellularly in host macrophages and has evolved diverse mechanisms to combat and survive oxidative stress. Here we show a novel F(420) -dependent anti-oxidant mechanism that protects Mtb against oxidative stress. Inactivation of the fbiC gene in Mtb results in a cofactor F(420) -deficient mutant that is hypersensitive to oxidative stress and exhibits a reduction in NADH/NAD(+) ratios upon treatment with menadione. In agreement with the recent hypothesis on oxidative stress being an important component of the pathway resulting in cell death by bactericidal agents, F(420) (-) mutants are hypersensitive to mycobactericidal agents such as isoniazid, moxifloxacin and clofazimine that elevate oxidative stress. The Mtb deazaflavin-dependent nitroreductase (Ddn) and its two homologues Rv1261c and Rv1558 encode for an F(420) H(2) -dependent quinone reductase (Fqr) function leading to dihydroquinones. We hypothesize that Fqr proteins catalyse an F(420) H(2) -specific obligate two-electron reduction of endogenous quinones, thereby competing with the one-electron reduction pathway and preventing the formation of harmful cytotoxic semiquinones, thus protecting mycobacteria against oxidative stress and bactericidal agents. These findings open up an avenue for the inhibition of the F(420) biosynthesis pathway or Fqr-class proteins as a mechanism to potentiate the action of bactericidal agents.
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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.