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Neutropenia increases the risk of life-threatening bacterial infections, a major cause of death in individuals with BTHS. Currently, there is no curative treatment for BTHS or associated neutropenia. The development of therapeutic strategies to correct BTHS-associated neutropenia has been hindered by a limited understanding of the underlying molecular mechanisms involved. BTHS is caused by a mutation in the\n                    <jats:italic>Tafazzin<\/jats:italic>\n                    gene encoding a transacylase required for the maturation of cardiolipin, an inner mitochondrial membrane phospholipid crucial for mitochondrial structure and function. We introduced a BTHS patient\u2019s point mutation (\n                    <jats:italic>TAZ<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>D75H<\/jats:italic>\n                    <\/jats:sup>\n                    ) into the mouse Tafazzin enzyme\u2019s critical acyltransferase site using\n                    <jats:italic>CRISPR\/Cas9<\/jats:italic>\n                    -mediated genome editing, resulting in a patient-tailored point mutant knock-in BTHS model (\n                    <jats:italic>Taz<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>D75H<\/jats:italic>\n                    <\/jats:sup>\n                    ) that expresses a stable mutant Taz\n                    <jats:sup>D75H<\/jats:sup>\n                    protein lacking transacylase activity.\n                    <jats:italic>Taz<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>D75H\u00a0<\/jats:italic>\n                    <\/jats:sup>\n                    mice were then used to investigate how loss of Tafazzin enzymatic activity impacts hematopoiesis. Male\n                    <jats:italic>Taz<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>D75H<\/jats:italic>\n                    <\/jats:sup>\n                    mice exhibited impaired granulopoiesis and neutropenia secondary to impaired function of hematopoietic progenitors. Furthermore, they demonstrated age-dependent neutrophil maturation impairment reflecting the variable neutropenia observed in BTHS patients. Additionally, male\n                    <jats:italic>Taz<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>D75H<\/jats:italic>\n                    <\/jats:sup>\n                    mice exhibit chronic lymphopenia that persists post\n                    <jats:italic>Taz<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>D75H<\/jats:italic>\n                    <\/jats:sup>\n                    bone marrow transplantation. Mechanistically, the\n                    <jats:italic>TAZ<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>D75H<\/jats:italic>\n                    <\/jats:sup>\n                    point mutation caused hematopoietic cell mitochondrial dysfunction in patient-derived immortalized\n                    <jats:italic>TAZ<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>D75H<\/jats:italic>\n                    <\/jats:sup>\n                    lymphoblasts, increasing reactive oxygen species production and mitochondrial membrane depolarization. Likewise, Cyclosporine A treatment rescued these mitochondrial phenotypes in vitro, confirming\n                    <jats:italic>TAZ<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>D75H<\/jats:italic>\n                    <\/jats:sup>\n                    mitochondrial dysfunction. Overall, our findings demonstrate that mitochondrial dysfunction secondary to TAFAZZIN loss of enzymatic function underlies BTHS-associated neutropenia and lymphopenia.\n                  <\/jats:p>","DOI":"10.1007\/s12015-025-10945-1","type":"journal-article","created":{"date-parts":[[2025,8,5]],"date-time":"2025-08-05T07:11:12Z","timestamp":1754377872000},"page":"2170-2187","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Granulopoietic Dysregulation in a Patient-Tailored Mouse Model of Barth Syndrome"],"prefix":"10.1007","volume":"21","author":[{"given":"Elizabeth A.","family":"Sierra Potchanant","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maegan L.","family":"Capitano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donna M.","family":"Edwards","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Baskar","family":"Ramdas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Scott","family":"Cooper","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James","family":"Ropa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S. 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Molecular Therapy, 28(12), 2621\u20132634.","journal-title":"Molecular Therapy"}],"updated-by":[{"DOI":"10.1007\/s12015-025-10983-9","type":"correction","label":"Correction","source":"publisher","updated":{"date-parts":[[2025,9,30]],"date-time":"2025-09-30T00:00:00Z","timestamp":1759190400000}}],"container-title":["Stem Cell Reviews and Reports"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/link.springer.com\/content\/pdf\/10.1007\/s12015-025-10945-1.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/link.springer.com\/article\/10.1007\/s12015-025-10945-1\/fulltext.html","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/link.springer.com\/content\/pdf\/10.1007\/s12015-025-10945-1.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2025,9,30]],"date-time":"2025-09-30T19:02:46Z","timestamp":1759258966000},"score":1,"resource":{"primary":{"URL":"https:\/\/link.springer.com\/10.1007\/s12015-025-10945-1"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2025,8,5]]},"references-count":78,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2025,10]]}},"alternative-id":["10945"],"URL":"https:\/\/doi.org\/10.1007\/s12015-025-10945-1","relation":{},"ISSN":["2629-3269","2629-3277"],"issn-type":[{"value":"2629-3269","type":"print"},{"value":"2629-3277","type":"electronic"}],"subject":[],"published":{"date-parts":[[2025,8,5]]},"assertion":[{"value":"11 July 2025","order":1,"name":"accepted","label":"Accepted","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"5 August 2025","order":2,"name":"first_online","label":"First Online","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"11 September 2025","order":3,"name":"change_date","label":"Change Date","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"Update","order":4,"name":"change_type","label":"Change Type","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"The original online version of this article was revised: The original published version of this article unfortunately contained a mistake. In this article, Simon J. Conway should have been denoted as a corresponding author. The error occurred during the typesetting and proofing process.","order":5,"name":"change_details","label":"Change Details","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"30 September 2025","order":6,"name":"change_date","label":"Change Date","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"Correction","order":7,"name":"change_type","label":"Change Type","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"A Correction to this paper has been published:","order":8,"name":"change_details","label":"Change Details","group":{"name":"ArticleHistory","label":"Article History"}},{"value":"https:\/\/doi.org\/10.1007\/s12015-025-10983-9","URL":"https:\/\/doi.org\/10.1007\/s12015-025-10983-9","order":9,"name":"change_details","label":"Change Details","group":{"name":"ArticleHistory","label":"Article History"}},{"order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Declarations"}},{"value":"All animal experiments were performed following the Guide for the Care and Use of Laboratory Animals published by the U.S. National Institutes of Health (Revised 2020) and were approved by the Indiana University School of Medicine Institutional Animal Care and Use Committee (Indianapolis, IN, USA). For cell line generation and collection of patient data, all procedures were conducted per the ethical standards of the responsible committee on human experimentation (institutional and national) and the tenets of the Declaration of Helsinki of 1975, as revised in 2013. Informed written consent was obtained from the patients and parents or legal guardians of all participants in the study.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics Approval"}},{"value":"All authors consent to publication.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent for Publication"}},{"value":"Not applicable.","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent to Participate"}},{"value":"The authors declare no competing interests.","order":5,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}]}}