Nature:“三亲婴儿”或在晚年出现健康问题
一项在小鼠身上开展的研究表明,所谓的“三亲婴儿”体内匹配错误的DNA可能导致以后的生活出现问题。相关成果日前发表于《自然》杂志。


一项在小鼠身上开展的研究表明,所谓的“三亲婴儿”体内匹配错误的DNA可能导致以后的生活出现问题。相关成果日前发表于《自然》杂志。

线粒体替代疗法于去年获英国议会批准,并且允许细胞“能量工厂”线粒体存在基因缺陷的女性,在不必将带有缺陷的线粒体DNA传递下去的情况下拥有孩子。

该疗法涉及将母亲卵子的细胞核或受精胚胎移植到不相关捐赠者的卵子内。由此生下的孩子将继承来自父母的核DNA,以及来自捐赠者的线粒体DNA。

不过,一项在小鼠身上开展的最新研究显示,线粒体DNA和核DNA之间的错配会加速衰老并影响到新陈代谢和肥胖。

来自西班牙国家心血管病研究中心的Jose Antonio Enriquez及其团队在小鼠身上获得了这一发现。研究人员专门培育了这些小鼠,使其拥有来自捐赠者的线粒体。当这些动物年幼时,它们的健康状况看上去不错。不过,随着小鼠变老,一系列问题开始出现,包括预示着衰老的染色体终端变短。

不过,目前尚不清楚相同的效应是否会在人类身上出现。这些试验中利用的小鼠是近亲交配的,而大多数人都是远系交配。如果在小鼠身上获得的这些发现同样发生在人类身上,那么这会令线粒体替代疗法极大地复杂化,因为找到其DNA同母亲拥有良好基因匹配的线粒体捐赠者将成为必需。

“就像器官移植和输血一样,选择线粒体捐赠者至关重要,以便使新的线粒体DNA从基因方面同母亲的DNA相似。”Enriquez表示。

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  • Mitochondrial and nuclear DNA matching shapes metabolism and healthy ageing

    Human mitochondrial DNA (mtDNA) shows extensive within-population sequence variability1. Many studies suggest that mtDNA variants may be associated with ageing or diseases2, 3, 4, although mechanistic evidence at the molecular level is lacking5, 6. Mitochondrial replacement has the potential to prevent transmission of disease-causing oocyte mtDNA. However, extension of this technology requires a comprehensive understanding of the physiological relevance of mtDNA sequence variability and its match with the nuclear-encoded mitochondrial genes. Studies in conplastic animals7, 8, 9 allow comparison of individuals with the same nuclear genome but different mtDNA variants, and have provided both supporting and refuting evidence that mtDNA variation influences organismal physiology. However, most of these studies did not confirm the conplastic status, focused on younger animals, and did not investigate the full range of physiological and phenotypic variability likely to be influenced by mitochondria. Here we systematically characterized conplastic mice throughout their lifespan using transcriptomic, proteomic, metabolomic, biochemical, physiological and phenotyping studies. We show that mtDNA haplotype profoundly influences mitochondrial proteostasis and reactive oxygen species generation, insulin signalling, obesity, and ageing parameters including telomere shortening and mitochondrial dysfunction, resulting in profound differences in health longevity between conplastic strains.

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