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首页> 外文期刊>PLoS Genetics >New Evidence Confirms That the Mitochondrial Bottleneck Is Generated without Reduction of Mitochondrial DNA Content in Early Primordial Germ Cells of Mice
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New Evidence Confirms That the Mitochondrial Bottleneck Is Generated without Reduction of Mitochondrial DNA Content in Early Primordial Germ Cells of Mice

机译：新证据证实线粒体瓶颈的产生没有降低小鼠原始生殖细胞中线粒体DNA的含量

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In mammals, observations of rapid shifts in mitochondrial DNA (mtDNA) variants between generations have led to the creation of the bottleneck theory for the transmission of mtDNA. The bottleneck could be attributed to a marked decline of mtDNA content in germ cells giving rise to the next generation, to a small effective number of mtDNA segregation units resulting from homoplasmic nucleoids rather than the single mtDNA molecule serving as the units of segregation, or to the selective transmission of a subgroup of the mtDNA population to the progeny. We have previously determined mtDNA copy number in single germ cells and shown that the bottleneck occurs without the reduction in germline mtDNA content. Recently one study suggested that the bottleneck is driven by a remarkable decline of mtDNA copies in early primordial germ cells (PGCs), while another study reported that the mtDNA genetic bottleneck results from replication of a subpopulation of the mtDNA genome during postnatal oocyte maturation and not during embryonic oogenesis, despite a detected a reduction in mtDNA content in early PGCs. To clarify these contradictory results, we examined the mtDNA copy number in PGCs isolated from transgenic mice expressing fluorescent proteins specifically in PGCs as in the aforementioned two other studies. We provide clear evidence to confirm that no remarkable reduction in mtDNA content occurs in PGCs and reinforce that the bottleneck is generated without reduction of mtDNA content in germ cells.
机译：在哺乳动物中，对线粒体DNA（mtDNA）变异在各代之间快速转换的观察导致了mtDNA传播的瓶颈理论的产生。瓶颈可能归因于生殖细胞中mtDNA含量的显着下降，从而导致了下一代;归因于同质核苷而不是单个mtDNA分子作为分离单位所导致的有效mtDNA分离单位数量少，或mtDNA群体的一个亚组选择性地传递给后代。我们先前已经确定了单个生殖细胞中的mtDNA拷贝数，并表明瓶颈发生而种系mtDNA含量却没有减少。最近，一项研究表明瓶颈是由早期原始生殖细胞（PGCs）中mtDNA拷贝的显着下降所驱动的，而另一项研究则报道了mtDNA遗传瓶颈是由产后卵母细胞成熟过程中mtDNA基因组亚群的复制引起的，而不是尽管在早期卵母细胞中检测到线粒体DNA含量降低，但在胚胎卵子发生过程中仍然存在。为了澄清这些矛盾的结果，我们检查了PGC中的mtDNA拷贝数，该PGC从转基因小鼠中特异性表达了PGC中的荧光蛋白，与上述两项其他研究一样。我们提供了明确的证据来确认PGC中mtDNA含量没有显着降低，并强化了产生瓶颈而不降低生殖细胞中mtDNA含量。

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