ArticleBiochimica et biophysica acta. Molecular and cell biology of lipids2019
Cardiolipin-deficient cells depend on anaplerotic pathways to ameliorate defective TCA cycle function.
Article in Biochimica et biophysica acta. Molecular and cell biology of lipids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Kog1 Represses Lipid Accumulation inJournal of fungi (Basel, Switzerland) · 2026Article
- The Metabolic Regulatory Mechanisms of Umami Amino Acids inFoods (Basel, Switzerland) · 2026Article
- A Saccharomyces cerevisiae knockout screen for genes critical for growth under sulfur- and nitrogen-limited conditions reveals intracellular sorting via vesicular transport systems.G3 (Bethesda, Md.) · 2025Article
- Barth Syndrome:Genes · 2025Review
- Perturbations in mitochondrial metabolism associated with defective cardiolipin biosynthesis: AnbioRxiv : the preprint server for biology · 2024Article
- NAD supplementation improves mitochondrial performance of cardiolipin mutants.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2022Article
- Cardiolipin function in the yeast S. cerevisiae and the lessons learned for Barth syndrome.Journal of inherited metabolic disease · 2022Review
- Studying Lipid-Related Pathophysiology Using the Yeast Model.Frontiers in physiology · 2021Review
- Metabolic Alterations Caused by Defective Cardiolipin Remodeling in Inherited Cardiomyopathies.Life (Basel, Switzerland) · 2020Review
- Loss of the mitochondrial lipid cardiolipin leads to decreased glutathione synthesis.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2020Article
- Cardiolipin-induced activation of pyruvate dehydrogenase links mitochondrial lipid biosynthesis to TCA cycle function.The Journal of biological chemistry · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Previous studies have shown that the cardiolipin (CL)-deficient yeast mutant, crd1Δ, has decreased levels of acetyl-CoA and decreased activities of the TCA cycle enzymes aconitase and succinate dehydrogenase. These biochemical phenotypes are expected to lead to defective TCA cycle function. In this study, we report that signaling and anaplerotic metabolic pathways that supplement defects in the TCA cycle are essential in crd1Δ mutant cells. The crd1Δ mutant is synthetically lethal with mutants in the TCA cycle, retrograde (RTG) pathway, glyoxylate cycle, and pyruvate carboxylase 1. Glutamate levels were decreased, and the mutant exhibited glutamate auxotrophy. Glyoxylate cycle genes were up-regulated, and the levels of glyoxylate metabolites succinate and citrate were increased in crd1Δ. Import of acetyl-CoA from the cytosol into mitochondria is essential in crd1Δ, as deletion of the carnitine-acetylcarnitine translocase led to lethality in the CL mutant. β-oxidation was functional in the mutant, and oleate supplementation rescued growth defects. These findings suggest that TCA cycle deficiency caused by the absence of CL necessitates activation of anaplerotic pathways to replenish acetyl-CoA and TCA cycle intermediates. Implications for Barth syndrome, a genetic disorder of CL metabolism, are discussed.
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