ArticleThe Journal of infectious diseases2010
Attenuation of Mycobacterium tuberculosis functionally disrupted in a fatty acyl-coenzyme A synthetase gene fadD5.
Article in The Journal of infectious diseases, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 64 citations in OpenAlex.
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- Trehalose Recycling Promotes Energy-Efficient Biosynthesis of the Mycobacterial Cell Envelope.mBio · 2021Article
- Genotypic and phenotypic diversity of Mycobacterium tuberculosis complex genotypes prevalent in West Africa.PloS one · 2021Article
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- Serum anti-Mce1A immunoglobulin detection as a tool for differential diagnosis of tuberculosis and latent tuberculosis infection in children and adolescents.Tuberculosis (Edinburgh, Scotland) · 2020Article
- Mammalian cell entry operons; novel and major subset candidates for diagnostics with special reference toThe veterinary quarterly · 2019Review
- Underestimated Manipulative Roles ofFrontiers in immunology · 2019Review
- Microenvironment ofBioMed research international · 2019Article
- Cholesterol and fatty acids grease the wheels of Mycobacterium tuberculosis pathogenesis.Pathogens and disease · 2018Review
- Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2018Review
- In silico analysis of class I adenylate-forming enzymes reveals family and group-specific conservations.PloS one · 2018Article
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Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
One key adaptation that Mycobacterium tuberculosis established to survive long term in vivo is a reliance on lipids as an energy source. M. tuberculosis H37Rv has 36 fadD genes annotated as putative fatty acyl-coenzyme A (CoA) synthetase genes, which encode enzymes that activate fatty acids for metabolism. One such gene, fadD5 (Rv0166), is located within the mce1 operon, a cluster of genes associated with M. tuberculosis persistence. We disrupted the putative fatty acid-binding site of fadD5 in H37Rv M. tuberculosis. No significant differences were found in the growth of the mutant and wild-type strains in vitro in nutrient-rich broth or in activated RAW264.7 cells. However, the fadD5 mutant was diminished in growth in minimal medium containing mycolic acid but not other long-chain fatty acids. C57BL/6 mice infected with the fadD5 mutant survived significantly longer than those infected with the wild type, and the mutant never attained the plateau phase of infection in mouse lungs. Infection in the steady-state phase was maintained for up to 168 days at a level that was 1-2 logs less than that noted in the wild type. These observations raise the rather intriguing possibility that FadD5 may serve to recycle mycolic acids for the long-term survival of the tubercle bacilli.
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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.