ArticlePhysiological reports2018
Drosophila tafazzin mutants have impaired exercise capacity.
Article in Physiological reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 18 citations in OpenAlex.
- Mitochondria-Homing Drug Mitochonic Acid 5 Improves Barth Syndrome Myopathy in a Human-Induced Pluripotent Stem Cell Model and Barth Syndrome Drosophila Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Cell cycle re-entry in the agingbioRxiv : the preprint server for biology · 2024Article
- Anomalous peroxidase activity of cytochrome c is the primary pathogenic target in Barth syndrome.Nature metabolism · 2023Article
- Article
- Phospholipids can regulate complex I assembly independent of their role in maintaining mitochondrial membrane integrity.Cell reports · 2023Article
- A novel panel of Drosophila TAFAZZIN mutants in distinct genetic backgrounds as a resource for therapeutic testing.PloS one · 2023Article
- Stimulating the sir2-spargel axis rescues exercise capacity and mitochondrial respiration in a Drosophila model of Barth syndrome.Disease models & mechanisms · 2022Article
- Endurance exercise ameliorates phenotypes ineLife · 2022Article
- Exercise and the Brain: Lessons From Invertebrate Studies.Frontiers in behavioral neuroscience · 2022Review
- Experimental models of Barth syndrome.Journal of inherited metabolic disease · 2022Review
- Phospholipids: Identification and Implication in Muscle Pathophysiology.International journal of molecular sciences · 2021Review
- Variation in mobility and exercise adaptations between Drosophila species.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2020Article
- Drosophila tafazzin mutants have impaired exercise capacity.Physiological reports · 2018Article
- Article
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3 authors at 1 institution in 1 country.
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Abstract
Cardiolipin (CL) is a mitochondrial phospholipid that helps maintain normal structure of the inner mitochondrial membrane and stabilize the protein complexes of the electron transport chain to promote efficient ATP synthesis. Tafazzin, an acyl-transferase, is required for synthesis of the mature form of CL. Mutations in the tafazzin (TAZ) gene are associated with a human disorder known as Barth syndrome. Symptoms of Barth syndrome often include muscle weakness and exercise intolerance. Previous work demonstrates that Drosophila Taz mutants exhibit motor weakness, as measured by reduced flying and climbing abilities. However, Drosophila TAZ mutants' baseline endurance or response to endurance exercise training has not been assessed. Here, we find that TAZ mutants have reduced endurance and do not improve following a stereotypical exercise training paradigm, indicating that loss of TAZ function leads to exercise intolerance in Drosophila. Although cardiac phenotypes are observed in human Barth syndrome patients, TAZ mutants had normal resistance to cardiac pacing. In the future, endurance may be a useful screening tool to identify additional genetic modifiers of tafazzin.
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