ArticlemBio2014
Triosephosphate isomerase is dispensable in vitro yet essential for Mycobacterium tuberculosis to establish infection.
Article in mBio, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 43 citations in OpenAlex.
- Mycobacterium tuberculosis IDH-PPARγ interaction suppresses GPX4 to drive macrophage ferroptosis and sustain persistent infection.Nature communications · 2026Article
- Metabolism-dependent succinylation governs resource allocation for antibiotic resistance.Science advances · 2025Article
- Repurposing of rabeprazole as an anti-Journal of enzyme inhibition and medicinal chemistry · 2023Article
- Sirtuin-dependent metabolic and epigenetic regulation of macrophages during tuberculosis.Frontiers in immunology · 2023Review
- Understanding the contribution of metabolism toFrontiers in cellular and infection microbiology · 2022Review
- Growth ofProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Essential Roles of PPARs in Lipid Metabolism during Mycobacterial Infection.International journal of molecular sciences · 2021Review
- Mycobacterial fatty acid catabolism is repressed by FdmR to sustain lipogenesis and virulence.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Mycobacterium tuberculosis infection is exacerbated in mice lacking lecithin:retinol acyltransferase.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- Two interacting ATPases protectJournal of bacteriology · 2020Article
- Derailing the aspartate pathway of Mycobacterium tuberculosis to eradicate persistent infection.Nature communications · 2019Article
- Comparing the Metabolic Capabilities of Bacteria in theMicroorganisms · 2019Review
- Arsenic Response of Three AltiplanicFrontiers in microbiology · 2019Article
- Metabolic principles of persistence and pathogenicity in Mycobacterium tuberculosis.Nature reviews. Microbiology · 2018Review
- Structures of the Mycobacterium tuberculosis GlpX protein (class II fructose-1,6-bisphosphatase): implications for the active oligomeric state, catalytic mechanism and citrate inhibition.Acta crystallographica. Section D, Structural biology · 2018Article
- Lipid metabolism and its implication in mycobacteria-host interaction.Current opinion in microbiology · 2018Review
- CitE Enzymes Are Essential forFrontiers in cellular and infection microbiology · 2018Article
- Identification of Enolase as the Target of 2-Aminothiazoles inFrontiers in microbiology · 2018Article
- Metabolic adaptation of two in silico mutants of Mycobacterium tuberculosis during infection.BMC systems biology · 2017Article
- Emerging Approaches to Tuberculosis Drug Development: At Home in the Metabolome.Trends in pharmacological sciences · 2017Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
ABSTRACT Triosephosphate isomerase (TPI) catalyzes the interconversion of dihydroxyacetone phosphate (DHAP) and glyceraldehyde-3-phosphate (G3P). This reaction is required for glycolysis and gluconeogenesis, and tpi has been predicted to be essential for growth of Mycobacterium tuberculosis. However, when studying a conditionally regulated tpi knockdown mutant, we noticed that depletion of TPI reduced growth of M. tuberculosis in media containing a single carbon source but not in media that contained both a glycolytic and a gluconeogenic carbon source. We used such two-carbon-source media to isolate a tpi deletion (Δtpi) mutant. The Δtpi mutant did not survive with single carbon substrates but grew like wild-type (WT) M. tuberculosis in the presence of both a glycolytic and a gluconeogenic carbon source. (13)C metabolite tracing revealed the accumulation of TPI substrates in Δtpi and the absence of alternative triosephosphate isomerases and metabolic bypass reactions, which confirmed the requirement of TPI for glycolysis and gluconeogenesis in M. tuberculosis. The Δtpi strain was furthermore severely attenuated in the mouse model of tuberculosis, suggesting that M. tuberculosis cannot simultaneously access sufficient quantities of glycolytic and gluconeogenic carbon substrates to establish infection in mice. IMPORTANCE The importance of central carbon metabolism for the pathogenesis of M. tuberculosis has recently been recognized, but the consequences of depleting specific metabolic enzymes remain to be identified for many enzymes. We investigated triosephosphate isomerase (TPI) because it is central to both glycolysis and gluconeogenesis and had been predicted to be essential for growth of M. tuberculosis. This work identified metabolic conditions that make TPI dispensable for M. tuberculosis growth in culture and proved that M. tuberculosis relies on a single TPI enzyme and has no metabolic bypass for the TPI-dependent interconversion of dihydroxyacetone phosphate and glyceraldehyde-3-phosphate in glycolysis and gluconeogenesis. Finally, we demonstrate that TPI is essential for growth of the pathogen in mouse lungs.
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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.