ArticleThe Journal of biological chemistry2014
Deletion of the cardiolipin-specific phospholipase Cld1 rescues growth and life span defects in the tafazzin mutant: implications for Barth syndrome.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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40 citing papers in PubMed, 65 citations in OpenAlex.
- Article
- Cardiolipin remodeling maintains the inner mitochondrial membrane in cells with saturated lipidomes.Journal of lipid research · 2024Article
- The phospholipids cardiolipin and phosphatidylethanolamine differentially regulate MDC biogenesis.The Journal of cell biology · 2024Article
- Genetic modifiers modulate phenotypic expression of tafazzin deficiency in a mouse model of Barth syndrome.Human molecular genetics · 2023Article
- Phenotypic Characterization of MaleBiomedicines · 2023Article
- Lifespan Extension ofInternational journal of molecular sciences · 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
- Role of cardiolipins, mitochondria, and autophagy in the differentiation process activated by all-trans retinoic acid in acute promyelocytic leukemia.Cell death & disease · 2022Article
- Current Knowledge on the Role of Cardiolipin Remodeling in the Context of Lipid Oxidation and Barth Syndrome.Frontiers in molecular biosciences · 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
- Fat of the Gut: Epithelial Phospholipids in Inflammatory Bowel Diseases.International journal of molecular sciences · 2021Review
- The Function of Tafazzin, a Mitochondrial Phospholipid-Lysophospholipid Acyltransferase.Journal of molecular biology · 2020Review
- Phospholipid ebb and flow makes mitochondria go.The Journal of cell biology · 2020Review
- The role of cardiolipin concentration and acyl chain composition on mitochondrial inner membrane molecular organization and function.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2019Review
- Mitochondrial dysfunctions in barth syndrome.IUBMB life · 2019Review
- Assembly of the complexes of oxidative phosphorylation triggers the remodeling of cardiolipin.Proceedings of the National Academy of Sciences of the United States of America · 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
- Aberrant cardiolipin metabolism is associated with cognitive deficiency and hippocampal alteration in tafazzin knockdown mice.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiolipin (CL) that is synthesized de novo is deacylated to monolysocardiolipin (MLCL), which is reacylated by tafazzin. Remodeled CL contains mostly unsaturated fatty acids. In eukaryotes, loss of tafazzin leads to growth and respiration defects, and in humans, this results in the life-threatening disorder Barth syndrome. Tafazzin deficiency causes a decrease in the CL/MLCL ratio and decreased unsaturated CL species. Which of these biochemical outcomes contributes to the physiological defects is not known. Yeast cells have a single CL-specific phospholipase, Cld1, that can be exploited to distinguish between these outcomes. The cld1Δ mutant has decreased unsaturated CL, but the CL/MLCL ratio is similar to that of wild type cells. We show that cld1Δ rescues growth, life span, and respiratory defects of the taz1Δ mutant. This suggests that defective growth and respiration in tafazzin-deficient cells are caused by the decreased CL/MLCL ratio and not by a deficiency in unsaturated CL. CLD1 expression is increased during respiratory growth and regulated by the heme activator protein transcriptional activation complex. Overexpression of CLD1 leads to decreased mitochondrial respiration and growth and instability of mitochondrial DNA. However, ATP concentrations are maintained by increasing glycolysis. We conclude that transcriptional regulation of Cld1-mediated deacylation of CL influences energy metabolism by modulating the relative contribution of glycolysis and respiration.
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