ArticleThe Journal of biological chemistry2016
Central Role of Pyruvate Kinase in Carbon Co-catabolism of Mycobacterium tuberculosis.
Article in The Journal of biological chemistry, 2016. 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, 50 citations in OpenAlex.
- A Key Metabolic Protein in Active Mycobacterium tuberculosis: Insights into Carbon, Nitrogen, and Sulfur Metabolism.Advances in experimental medicine and biology · 2026Review
- Transcriptional analysis of genes associated with glycolysis in Streptomyces coelicolor M145.International microbiology : the official journal of the Spanish Society for Microbiology · 2025Article
- Mycobacterium tuberculosis curli pili (MTP) and heparin-binding hemagglutinin adhesin (HBHA) facilitate regulation of central carbon metabolism, enhancement of ATP synthesis and cell wall biosynthesis.Archives of microbiology · 2025Article
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- Bactericidal bissulfone BScience China. Life sciences · 2024Article
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- Phenotypic adaptation ofFrontiers in cellular and infection microbiology · 2022Review
- Metabolic fluxes for nutritional flexibility of Mycobacterium tuberculosis.Molecular systems biology · 2021Article
- Phosphofructokinases A and B fromInternational journal of molecular sciences · 2021Article
- Structure, Function and Regulation of a Second Pyruvate Kinase Isozyme inFrontiers in microbiology · 2021Article
- Bedaquiline reprograms central metabolism to reveal glycolytic vulnerability in Mycobacterium tuberculosis.Nature communications · 2020Article
- Model-based integration of genomics and metabolomics reveals SNP functionality inProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Derailing the aspartate pathway of Mycobacterium tuberculosis to eradicate persistent infection.Nature communications · 2019Article
- Review
- PPE37 Is Essential forInfection and immunity · 2019Article
- Mycobacterium tuberculosis carrying a rifampicin drug resistance mutation reprograms macrophage metabolism through cell wall lipid changes.Nature microbiology · 2018Article
- Metabolic principles of persistence and pathogenicity in Mycobacterium tuberculosis.Nature reviews. Microbiology · 2018Review
- Glutamate mediated metabolic neutralization mitigates propionate toxicity in intracellular Mycobacterium tuberculosis.Scientific reports · 2018Article
- Untargeted metabolomics reveals a new mode of action of pretomanid (PA-824).Scientific reports · 2018Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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Abstract
Mycobacterium tuberculosis (Mtb) displays a high degree of metabolic plasticity to adapt to challenging host environments. Genetic evidence suggests thatMtbrelies mainly on fatty acid catabolism in the host. However,Mtbalso maintains a functional glycolytic pathway and its role in the cellular metabolism ofMtbhas yet to be understood. Pyruvate kinase catalyzes the last and rate-limiting step in glycolysis and theMtbgenome harbors one putative pyruvate kinase (pykA, Rv1617). Here we show thatpykAencodes an active pyruvate kinase that is allosterically activated by glucose 6-phosphate (Glc-6-P) and adenosine monophosphate (AMP). Deletion ofpykApreventsMtbgrowth in the presence of fermentable carbon sources and has a cidal effect in the presence of glucose that correlates with elevated levels of the toxic catabolite methylglyoxal. Growth attenuation was also observed in media containing a combination of short chain fatty acids and glucose and surprisingly, in media containing odd and even chain fatty acids alone. Untargeted high sensitivity metabolomics revealed that inactivation of pyruvate kinase leads to accumulation of phosphoenolpyruvate (P-enolpyruvate), citrate, and aconitate, which was consistent with allosteric inhibition of isocitrate dehydrogenase by P-enolpyruvate. This metabolic block could be relieved by addition of the α-ketoglutarate precursor glutamate. Taken together, our study identifies an essential role of pyruvate kinase in preventing metabolic block during carbon co-catabolism inMtb.
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