Mitochondrial genome inheritance and replacement in the human germline. (5th July 2017)

• Record Type: Journal Article
• Authors: Wolf, Don P; Hayama, Tomonari; Mitalipov, Shoukhrat
• Is Part Of: EMBO journal. Volume 36:Number 15(2017)
• Page Start: 2177
• Page End: 2181
• Publication Date: 2017-07-05
• Subjects: Molecular biology -- Periodicals; 572.805
• DOI: 10.15252/embj.201797606
• Languages: English
• ISSNs: 0261-4189

Abstract

Abstract : Mitochondria, the ubiquitous power packs in nearly every eukaryotic cell, contain their own DNA, known as mtDNA, which is inherited exclusively from the mother. The number of mitochondrial genomes varies depending on the cell's energy needs. The mature oocyte contains the highest number of mitochondria of any cell type, although there is little if any mtDNA replication after fertilization until the embryo implants. This has potential repercussions for mitochondrial replacement therapy (MRT; see description of currently employed methods below) used to prevent the transmission of mtDNA‐based disorders. If only a few mitochondria with defective mtDNA are left in the embryo and undergo extensive replication, it might therefore thwart the purpose of MRT. In order to improve the safety and efficacy of this experimental therapy, we need a better understanding of how and which mtDNA is tagged for replication versus transcription after fertilization of the oocyte. Abstract : Mitochondrial replacement therapy aims to prevent the transmission of mitochondrial‐linked diseases by exchanging maternal mitochondria with healthy ones. To improve its safety and efficiency, it is vital to understand how and which mitochondrial genomes of the oocyte are tagged for replication in the growing embryo.