ArticleNature communications2024
Dependency on host vitamin B12 has shaped Mycobacterium tuberculosis Complex evolution.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- MetF-Dependent Methionine Biosynthesis Is Required for Mycobacterium tuberculosis Survival and In Vivo Persistence.MicrobiologyOpen · 2026Article
- Mycobacterium tuberculosis VadK is required for the regulation of the methylcitrate cycle and virulence.EMBO reports · 2026Article
- The metallophosphoesterase Rv0805 regulates carbon flux and cell envelope homeostasis during growth of mycobacteria in propionate.Journal of bacteriology · 2026Article
- Vitamin B12 promotes cefiderocol resistance and small-colony variants in carbapenem-resistantmBio · 2026Article
- Article
- Cobamide metabolism, regulation, and adaptation inJournal of bacteriology · 2025Review
- Genome graphs reveal the importance of structural variation in Mycobacterium tuberculosis evolution and drug resistance.Nature communications · 2025Article
- VadK, a Non-Canonical Kinase that Regulates the Methylcitrate Cycle and is Essential forbioRxiv : the preprint server for biology · 2025Article
- Genome-wide phenotypic insights into mycobacterial virulence using Drosophila melanogaster.PLoS pathogens · 2025Article
- A transcriptional plasticity-aware framework for RNA-seq differential expression analysis.Briefings in bioinformatics · 2025Article
- Evolutionary Trajectories of Methionine Metabolism in Mycobacterium and Its Application to Engineer a Vitamin B12 Whole-Cell Ribosensor.Microbial biotechnology · 2025Article
- Nutritional Deficiencies and Management in Tuberculosis: Pharmacotherapeutic and Clinical Implications.Nutrients · 2025Review
- Impaired fatty acid import or catabolism in macrophages restricts intracellular growth ofeLife · 2025Article
- Micronutrient-deficient diets and possible environmental enteric dysfunction in Buruli ulcer endemic communities in Ghana: Lower dietary diversity and reduced serum zinc and vitamin C implicate micronutrient status a possible susceptibility factor.PLoS neglected tropical diseases · 2025Article
- Impaired fatty acid import or catabolism in macrophages restricts intracellular growth ofbioRxiv : the preprint server for biology · 2025Article
- Flavin and deazaflavin biosynthesis in mycobacteria: relevance to physiology, implications for drug discovery, MR-1 antigenicity, and vaccine development.Frontiers in immunology · 2025Review
- MetE: a promising protective antigen for tuberculosis vaccine development.Frontiers in immunology · 2025Article
- A novel regulatory interplay between atypical B12 riboswitches and uORF translation in Mycobacterium tuberculosis.Nucleic acids research · 2024Article
- Identification of Rv1133c (MetE) as a marker ofFrontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Human and animal tuberculosis is caused by the Mycobacterium tuberculosis Complex (MTBC), which has evolved a genomic decay of cobalamin (vitamin B12) biosynthetic genes. Accordingly, and in sharp contrast to environmental, opportunistic and ancestor mycobacteria; we demonstrate that M. tuberculosis (Mtb), M. africanum, and animal-adapted lineages, lack endogenous production of cobalamin, yet they retain the capacity for exogenous uptake. A B12 anemic model in immunocompromised and immunocompetent mice, demonstrates improved survival, and lower bacteria in organs, in B12 anemic animals infected with Mtb relative to non-anemic controls. Conversely, no differences were observed between mice groups infected with M. canettii, an ancestor mycobacterium which retains cobalamin biosynthesis. Interrogation of the B12 transcriptome in three MTBC strains defined L-methionine synthesis by metE and metH genes as a key phenotype. Expression of metE is repressed by a cobalamin riboswitch, while MetH requires the cobalamin cofactor. Thus, deletion of metE predominantly attenuates Mtb in anemic mice; although inactivation of metH exclusively causes attenuation in non-anemic controls. Here, we show how sub-physiological levels of B12 in the host antagonizes Mtb virulence, and describe a yet unknown mechanism of host-pathogen cross-talk with implications for B12 anemic populations.
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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.