ArticlePLoS biology2023
A D-2-hydroxyglutarate dehydrogenase mutant reveals a critical role for ketone body metabolism in Caenorhabditis elegans development.
Article in PLoS biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Quantifying Embryonic Lethality Rate in Caenorhabditis elegans.Journal of visualized experiments : JoVE · 2026Article
- Zinc excess promotes lysosome remodeling by activating HLH-30/TFEB through the action of the high zinc sensor HIZR-1.bioRxiv : the preprint server for biology · 2026Article
- Shared urinary metabolomic signatures as potential biomarkers for early intestinalCurrent research in parasitology & vector-borne diseases · 2026Article
- Distinct S-adenosylmethionine synthases link phosphatidylcholine to mitochondrial function and stress survival.PLoS biology · 2025Article
- Stereochemistry and Charged State Influence Effector Outcomes of d-2-Hydroxyglutarate Dehydrogenase Ligands.Biochemistry · 2025Article
- New alleles of D-2-hydroxyglutarate dehydrogenase enable studies of oncometabolite function in Drosophila melanogaster.G3 (Bethesda, Md.) · 2025Article
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- Phytochemical-richFrontiers in nutrition · 2025Article
- Article
- Host-microbe interactions rewire metabolism in a C. elegans model of leucine breakdown deficiency.Nature metabolism · 2024Article
- Systems-level transcriptional regulation of Caenorhabditis elegans metabolism.Molecular systems biology · 2023Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
In humans, mutations in D-2-hydroxyglutarate (D-2HG) dehydrogenase (D2HGDH) result in D-2HG accumulation, delayed development, seizures, and ataxia. While the mechanisms of 2HG-associated diseases have been studied extensively, the endogenous metabolism of D-2HG remains unclear in any organism. Here, we find that, in Caenorhabditis elegans, D-2HG is produced in the propionate shunt, which is transcriptionally activated when flux through the canonical, vitamin B12-dependent propionate breakdown pathway is perturbed. Loss of the D2HGDH ortholog, dhgd-1, results in embryonic lethality, mitochondrial defects, and the up-regulation of ketone body metabolism genes. Viability can be rescued by RNAi of hphd-1, which encodes the enzyme that produces D-2HG or by supplementing either vitamin B12 or the ketone bodies 3-hydroxybutyrate (3HB) and acetoacetate (AA). Altogether, our findings support a model in which C. elegans relies on ketone bodies for energy when vitamin B12 levels are low and in which a loss of dhgd-1 causes lethality by limiting ketone body production.
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