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By employing an mtDNA mutator (Polgm) mouse model, we found the fetal growth retardation and placental dysfunction in post-implantation embryos derived from Polgm oocytes. Remarkably, Polgm oocytes displayed the global loss of DNA methylation; following fertilization, zygotic genome experienced insufficient demethylation, along with dysregulation of gene expression. Spindle\u2013chromosome exchange experiment revealed that cytoplasmic factors in Polgm oocytes are responsible for such a deficient epigenetic remodeling. Moreover, metabolomic profiling identified a significant reduction in the \u03b1-ketoglutarate (\u03b1KG) level in oocytes from Polgm mice. Importantly, \u03b1KG supplement restored both DNA methylation state and transcriptional activity in Polgm embryos, consequently preventing the developmental defects. Our findings uncover the important role of oocyte mtDNA mutation in controlling epigenetic reprogramming and gene expression during embryogenesis. \u03b1KG deserves further evaluation as a potential drug for treating mitochondrial dysfunction-related fertility decline.<\/jats:p>","DOI":"10.1093\/nsr\/nwac136","type":"journal-article","created":{"date-parts":[[2022,7,13]],"date-time":"2022-07-13T18:19:09Z","timestamp":1657736349000},"source":"Crossref","is-referenced-by-count":23,"title":["Increased mtDNA mutation frequency in oocytes causes epigenetic alterations and embryonic defects"],"prefix":"10.1093","volume":"9","author":[{"given":"Longsen","family":"Han","sequence":"first","affiliation":[{"name":"State Key Laboratory of Reproductive Medicine, Suzhou Municipal Hospital, Nanjing Medical University , Nanjing 211166 , China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yujia","family":"Chen","sequence":"additional","affiliation":[{"name":"State Key Laboratory of 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