异质性
生物
线粒体DNA
遗传学
否定选择
瓶颈
非孟德尔遗传
等位基因
突变
传输(电信)
表型
粒线体疾病
突变
突变体
线粒体
选择(遗传算法)
自噬
DNA
进化生物学
遗传(遗传算法)
基因组
人口瓶颈
细胞生物学
人类线粒体遗传学
症候群
模式生物
点突变
遗传变异
机制(生物学)
计算生物学
作者
Laura Sophie Kremer,Zoe J. Golder,Tom Barton-Owen,Polyxeni Papadea,Camilla Koolmeister,Patrick Francis Chinnery,Nils‐Göran Larsson
出处
期刊:Science Advances
[American Association for the Advancement of Science]
日期:2025-11-12
卷期号:11 (46): eaea4660-eaea4660
被引量:6
标识
DOI:10.1126/sciadv.aea4660
摘要
Mammalian mitochondrial DNA (mtDNA) inheritance differs fundamentally from nuclear inheritance owing to exclusive maternal transmission, high mutation rate, and lack of recombination. Two key mechanisms shape this inheritance: the bottleneck, which drives stochastic transmission of maternal mtDNA variants, and purifying selection, which actively removes mutant mtDNA. Whether these mechanisms interact has been unresolved. To address this question, we generated a series of mouse models with random mtDNA mutations alongside alleles altering mtDNA copy number or decreasing autophagy. We demonstrate that tightening the mtDNA bottleneck increases heteroplasmic variance between individuals, causing lower mutational burden and nonsynonymous-to-synonymous ratios. In contrast, reduced autophagy weakens purifying selection, leading to decreased interoffspring heteroplasmic variance and increased mutational burden with higher nonsynonymous-to-synonymous ratios. These findings provide experimental evidence that the mtDNA bottleneck size modulates the efficacy of purifying selection. Our findings yield fundamental insights into the processes governing mammalian mtDNA transmission with direct implications for the origin and propagation of mtDNA mutations causing human disease.
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