ArticleThe Journal of biological chemistry2017
Loss of Cardiolipin Leads to Perturbation of Acetyl-CoA Synthesis.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Barth Syndrome:Genes · 2025Review
- Lithium compromises the bioenergetic reserve of cardiomyoblasts mitochondria.Journal of bioenergetics and biomembranes · 2025Article
- Perturbations in mitochondrial metabolism associated with defective cardiolipin biosynthesis: AnbioRxiv : the preprint server for biology · 2024Article
- Upregulation of the AMPK-FOXO1-PDK4 pathway is a primary mechanism of pyruvate dehydrogenase activity reduction in tafazzin-deficient cells.Scientific reports · 2024Article
- Review
- Predicting and explaining the impact of genetic disruptions and interactions on organismal viability.Bioinformatics (Oxford, England) · 2022Article
- Barth Syndrome Cardiomyopathy: An Update.Genes · 2022Review
- 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
- Experimental models of Barth syndrome.Journal of inherited metabolic disease · 2022Review
- Metabolomics and lipidomics in Caenorhabditis elegans using a single-sample preparation.Disease models & mechanisms · 2021Article
- Studying Lipid-Related Pathophysiology Using the Yeast Model.Frontiers in physiology · 2021Review
- Cardiolipin, the Mitochondrial Signature Lipid: Implication in Cancer.International journal of molecular sciences · 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
- Cardiolipin-deficient cells depend on anaplerotic pathways to ameliorate defective TCA cycle function.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2019Article
- Overexpression of branched-chain amino acid aminotransferases rescues the growth defects of cells lacking the Barth syndrome-related gene TAZ1.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Genetic re-engineering of polyunsaturated phospholipid profile of Saccharomyces cerevisiae identifies a novel role for Cld1 in mitigating the effects of cardiolipin peroxidation.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018Article
- Review
- Drosophila tafazzin mutants have impaired exercise capacity.Physiological reports · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Cardiolipin (CL), the signature phospholipid of mitochondrial membranes, plays an important role in mitochondrial processes and bioenergetics. CL is synthesized de novo and undergoes remodeling in the mitochondrial membranes. Perturbation of CL remodeling leads to the rare X-linked genetic disorder Barth syndrome, which shows disparities in clinical presentation. To uncover biochemical modifiers that exacerbate CL deficiency, we carried out a synthetic genetic array screen to identify synthetic lethal interactions with the yeast CL synthase mutant crd1Δ. The results indicated that crd1Δ is synthetically lethal with mutants in pyruvate dehydrogenase (PDH), which catalyzes the conversion of pyruvate to acetyl-CoA. Acetyl-CoA levels were decreased in the mutant. The synthesis of acetyl-CoA depends primarily on the PDH-catalyzed conversion of pyruvate in the mitochondria and on the PDH bypass in the cytosol, which synthesizes acetyl-CoA from acetate. Consistent with perturbation of the PDH bypass, crd1Δ cells grown on acetate as the sole carbon source exhibited decreased growth, decreased acetyl-CoA, and increased intracellular acetate levels resulting from decreased acetyl-CoA synthetase activity. PDH mRNA and protein levels were up-regulated in crd1Δ cells, but PDH enzyme activity was not increased, indicating that PDH up-regulation did not compensate for defects in the PDH bypass. These findings demonstrate for the first time that CL is required for acetyl-CoA synthesis, which is decreased in CL-deficient cells as a result of a defective PDH bypass pathway.
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