ArticleNature communications2024
A universal metabolite repair enzyme removes a strong inhibitor of the TCA cycle.
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 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Orphan Enzymes in the Mammalian L-Fucose Degradation Pathway.Biomolecules · 2026Review
- The Preservation of Muscle Mitochondrial Machinery During Hypometabolic Hibernation in Scandinavian Brown Bears (Ursus arctos).Acta physiologica (Oxford, England) · 2026Article
- Massive-scale single-nucleus multi-omics identifies novel rare noncoding drivers of Parkinson's disease.bioRxiv : the preprint server for biology · 2026Article
- Metabolomic effects of total flavone of Abelmoschus manihot (L.) medik. on patients with radiation-induced heart disease.Scientific reports · 2025Article
- Mutations Elevate an Underground Pathway to a Physiologically Relevant Protopathway.Molecular biology and evolution · 2025Article
- FAHD1 and mitochondrial metabolism: a decade of pioneering discoveries.The FEBS journal · 2025Review
- α-Amino-β-carboxymuconate-ε-semialdehyde decarboxylase catalyzes enol/keto tautomerization of oxaloacetate.The Journal of biological chemistry · 2024Article
- Identification of age-associated microbial changes via long-read 16S sequencing.Gut pathogens · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
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Abstract
A prevalent side-reaction of succinate dehydrogenase oxidizes malate to enol-oxaloacetate (OAA), a metabolically inactive form of OAA that is a strong inhibitor of succinate dehydrogenase. We purified from cow heart mitochondria an enzyme (OAT1) with OAA tautomerase (OAT) activity that converts enol-OAA to the physiological keto-OAA form, and determined that it belongs to the highly conserved and previously uncharacterized Fumarylacetoacetate_hydrolase_domain-containing protein family. From all three domains of life, heterologously expressed proteins were shown to have strong OAT activity, and ablating the OAT1 homolog caused significant growth defects. In Escherichia coli, expression of succinate dehydrogenase was necessary for OAT1-associated growth defects to occur, and ablating OAT1 caused a significant increase in acetate and other metabolites associated with anaerobic respiration. OAT1 increased the succinate dehydrogenase reaction rate by 35% in in vitro assays with physiological concentrations of both succinate and malate. Our results suggest that OAT1 is a universal metabolite repair enzyme that is required to maximize aerobic respiration efficiency by preventing succinate dehydrogenase inhibition.
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