ArticlePloS one2015
Mouse Tafazzin Is Required for Male Germ Cell Meiosis and Spermatogenesis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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The trial behind it
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Ebselen restores mitochondrial function through metabolic rewiring in Barth syndrome and related mitochondrial diseases.EMBO molecular medicine · 2026Article
- Cardiolipin preserves TNature metabolism · 2026Article
- The Loss of Tafazzin Transacetylase Activity Is Sufficient to Drive Testicular Infertility.Journal of developmental 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
- Mitochondrial defects caused by PARL deficiency lead to arrested spermatogenesis and ferroptosis.eLife · 2023Article
- A new murine model of Barth syndrome neutropenia links TAFAZZIN deficiency to increased ER stress-induced apoptosis.Blood advances · 2022Article
- Barth Syndrome Cardiomyopathy: An Update.Genes · 2022Review
- Experimental models of Barth syndrome.Journal of inherited metabolic disease · 2022Review
- Dynamic Cardiolipin Synthesis Is Required for CD8Cell metabolism · 2020Article
- Role ofJournal of developmental biology · 2020Review
- AAV Gene Therapy Prevents and Reverses Heart Failure in a Murine Knockout Model of Barth Syndrome.Circulation research · 2020Article
- Mitochondrial dysfunctions in barth syndrome.IUBMB life · 2019Review
- Imbalanced mitochondrial function provokes heterotaxy via aberrant ciliogenesis.The Journal of clinical investigation · 2019Article
- Extramitochondrial cardiolipin suggests a novel function of mitochondria in spermatogenesis.The Journal of cell biology · 2019Article
- Mitochondria maintain controlled activation state of epithelial-resident T lymphocytes.Science immunology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Barth syndrome is an X-linked mitochondrial disease, symptoms of which include neutropenia and cardiac myopathy. These symptoms are the most significant clinical consequences of a disease, which is increasingly recognised to have a variable presentation. Mutation in the Taz gene in Xq28 is thought to be responsible for the condition, by altering mitochondrial lipid content and mitochondrial function. Male chimeras carrying a targeted mutation of Taz on their X-chromosome were infertile. Testes from the Taz knockout chimeras were smaller than their control counterparts and this was associated with a disruption of the progression of spermatocytes through meiosis to spermiogenesis. Taz knockout ES cells also showed a defect when differentiated to germ cells in vitro. Mutant spermatocytes failed to progress past the pachytene stage of meiosis and had higher levels of DNA double strand damage and increased levels of endogenous retrotransposon activity. Altogether these data revealed a novel role for Taz in helping to maintain genome integrity in meiosis and facilitating germ cell differentiation. We have unravelled a novel function for the Taz protein, which should contribute to an understanding of how a disruption of the Taz gene results in the complex symptoms underlying Barth Syndrome.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.