Segregation of mitochondrial DNA heteroplasmy through a developmental genetic bottleneck in human embryos

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Extreme-Depth Re-sequencing of Mitochondrial DNA Finds No Evidence of Paternal Transmission in Humans

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Selective propagation of functional mitochondrial DNA during oogenesis restricts the transmission of a deleterious mitochondrial variant

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PINK1-Phosphorylated Mitofusin 2 Is a Parkin Receptor for Culling Damaged Mitochondria

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Ultra-Sensitive Sequencing Reveals an Age-Related Increase in Somatic Mitochondrial Mutations That Are Inconsistent with Oxidative Damage

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Variation in germline mtDNA heteroplasmy is determined prenatally but modified during subsequent transmission

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Previous Estimates of Mitochondrial DNA Mutation Level Variance Did Not Account for Sampling Error: Comparing the mtDNA Genetic Bottleneck in Mice and Humans

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Pronuclear transfer in human embryos to prevent transmission of mitochondrial DNA disease

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PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin

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The mitochondrial DNA genetic bottleneck results from replication of a subpopulation of genomes

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A reduction of mitochondrial DNA molecules during embryogenesis explains the rapid segregation of genotypes

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Purifying selection of mtDNA and its implications for understanding evolution and mitochondrial disease

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Strong Purifying Selection in Transmission of Mammalian Mitochondrial DNA

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