ArticleNature communications2021
Multiple acyl-CoA dehydrogenase deficiency kills Mycobacterium tuberculosis in vitro and during infection.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- An adenylyl cyclase switch reroutes carbon from growth to virulence lipids inbioRxiv : the preprint server for biology · 2026Article
- Mycobacterium tuberculosis long-chain fatty acid resistome reveals universal stress protein TB15.3 as essential for infection.Communications biology · 2026Article
- Structural basis for EtfD-mediated coupling of β-oxidation and the respiratory chain in mycobacteria.The EMBO journal · 2026Article
- Granuloma dual RNA-seq reveals composite transcriptional programs driven by neutrophils and necrosis within tuberculous granulomas.Science advances · 2026Article
- A Key Metabolic Protein in Active Mycobacterium tuberculosis: Insights into Carbon, Nitrogen, and Sulfur Metabolism.Advances in experimental medicine and biology · 2026Review
- Cell envelope maintenance by PhoP is essential forProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Essential redundancies fuel Mycobacterium tuberculosis adaptation to the host.PLoS pathogens · 2025Review
- Genomic characterisation of recurrent Mycobacterium avium isolates from chronically infected patients reveals patterns of within-host evolution.Genome medicine · 2025Article
- Phloretin-nanospanlastics for targeting the Akt/PI3K signaling pathways in dimethylhydrazine-induced colon cancer in mice.International journal of pharmaceutics: X · 2025Article
- Genome-Wide Identification and Functional Characterization of the Acyl-CoA Dehydrogenase (ACAD) Family inInternational journal of molecular sciences · 2025Article
- Flavin and deazaflavin biosynthesis in mycobacteria: relevance to physiology, implications for drug discovery, MR-1 antigenicity, and vaccine development.Frontiers in immunology · 2025Review
- Universal Lineage-Independent Markers of Multidrug Resistance inMicroorganisms · 2024Article
- Inhibitors of the Thioesterase Activity ofACS infectious diseases · 2024Article
- Iron-related gene mutations driving global Mycobacterium tuberculosis transmission revealed by whole-genome sequencing.BMC genomics · 2024Article
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- Optimization of Phloretin-loaded Nanospanlastics for Targeting ofCurrent pharmaceutical biotechnology · 2024Article
- MceG stabilizes the Mce1 and Mce4 transporters in Mycobacterium tuberculosis.The Journal of biological chemistry · 2023Article
- Systematic analysis of lysine crotonylation in human macrophages responding to MRSA infection.Frontiers in cellular and infection microbiology · 2023Article
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Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The human pathogen Mycobacterium tuberculosis depends on host fatty acids as a carbon source. However, fatty acid β-oxidation is mediated by redundant enzymes, which hampers the development of antitubercular drugs targeting this pathway. Here, we show that rv0338c, which we refer to as etfD, encodes a membrane oxidoreductase essential for β-oxidation in M. tuberculosis. An etfD deletion mutant is incapable of growing on fatty acids or cholesterol, with long-chain fatty acids being bactericidal, and fails to grow and survive in mice. Analysis of the mutant's metabolome reveals a block in β-oxidation at the step catalyzed by acyl-CoA dehydrogenases (ACADs), which in other organisms are functionally dependent on an electron transfer flavoprotein (ETF) and its cognate oxidoreductase. We use immunoprecipitation to show that M. tuberculosis EtfD interacts with FixA (EtfB), a protein that is homologous to the human ETF subunit β and is encoded in an operon with fixB, encoding a homologue of human ETF subunit α. We thus refer to FixA and FixB as EtfB and EtfA, respectively. Our results indicate that EtfBA and EtfD (which is not homologous to human EtfD) function as the ETF and oxidoreductase for β-oxidation in M. tuberculosis and support this pathway as a potential target for tuberculosis drug development.
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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.