The mitochondrial bottleneck occurs without reduction of mtDNA content in female mouse germ cells

@article{Cao2007TheMB,
  title={The mitochondrial bottleneck occurs without reduction of mtDNA content in female mouse germ cells},
  author={Liqin Cao and Hiroshi Shitara and Takuro Horii and Yasumitsu Nagao and Hiroshi Imai and Kuniya Abe and Takahiko Hara and Jun-ichi Hayashi and Hiromichi Yonekawa},
  journal={Nature Genetics},
  year={2007},
  volume={39},
  pages={386-390}
}
Observations of rapid shifts in mitochondrial DNA (mtDNA) variants between generations prompted the creation of the bottleneck theory. A prevalent hypothesis is that a massive reduction in mtDNA content during early oogenesis leads to the bottleneck. To test this, we estimated the mtDNA copy number in single germline cells and in single somatic cells of early embryos in mice. Primordial germ cells (PGCs) show consistent, moderate mtDNA copy numbers across developmental stages, whereas primary… 
New Evidence Confirms That the Mitochondrial Bottleneck Is Generated without Reduction of Mitochondrial DNA Content in Early Primordial Germ Cells of Mice
TLDR
Clear evidence is provided to confirm that no remarkable reduction in mt DNA content occurs in PGCs and reinforce that the bottleneck is generated without reduction of mtDNA content in germ cells.
A reduction of mitochondrial DNA molecules during embryogenesis explains the rapid segregation of genotypes
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It is shown that the partitioning of mtDNA molecules into different cells before and after implantation, followed by the segregation of replicating mtDNA between proliferating primordial germ cells, is responsible for the different levels of heteroplasmy seen in the offspring ofheteroplasmic female mice.
The mitochondrial DNA genetic bottleneck results from replication of a subpopulation of genomes
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By directly tracking the evolution of mtDNA genotypic variance during oogenesis, it is shown that the genetic bottleneck occurs during postnatal folliculogenesis and not during embryonic oogenesis.
Segregation of mitochondrial DNA heteroplasmy through a developmental genetic bottleneck in human embryos
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It is shown that mtDNA copy number is reduced and non-synonymous mt DNA mutations are eliminated to prevent mtDNA mutation accumulation in germ cells during human primordial germ cell development, preventing the relentless accumulation of mtDNA mutations in the human population predicted by Muller’s ratchet.
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It is shown that PGCs generate a bottleneck in mtDNA number by segregating mitochondria into lobe-like protrusions that are cannibalized by adjacent cells, reducing mtDNA content two-fold, and that the kinase PINK1, operating independently of Parkin and autophagy, preferentially reduces the fraction of mutant mtDNAs.
Oxygen tension modulates the mitochondrial genetic bottleneck and influences the segregation of a heteroplasmic mtDNA variant in vitro
TLDR
Differences in oxygen tension occurring during early development likely modulate the amount of mtDNA, facilitating mtDNA segregation and contributing to tissue-specific mutation loads.
Transmission of Mitochondrial DNA Diseases and Ways to Prevent Them
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New evidence that some types of deleterious mtDNA mutations are eliminated within a few generations suggests that women undergoing PGD have a reasonable chance of generating embryos with a lower mutant load than their own.
What cost mitochondria? The maintenance of functional mitochondrial DNA within and across generations
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The consequences of life-history differences among taxa with respect to mtDNA evolution are discussed and a case for the use of microorganisms to experimentally manipulate levels of selection is made.
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