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线粒体、母系遗传和不对称适应度:为什么男性寿命更短。

Mitochondria, maternal inheritance, and asymmetric fitness: why males die younger.

机构信息

School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW, Australia.

出版信息

Bioessays. 2013 Feb;35(2):93-9. doi: 10.1002/bies.201200141. Epub 2012 Dec 27.

DOI:10.1002/bies.201200141
PMID:23281153
Abstract

Mitochondrial function is achieved through the cooperative interaction of two genomes: one nuclear (nuDNA) and the other mitochondrial (mtDNA). The unusual transmission of mtDNA, predominantly maternal without recombination is predicted to affect the fitness of male offspring. Recent research suggests the strong sexual dimorphism in aging is one such fitness consequence. The uniparental inheritance of mtDNA results in a selection asymmetry; mutations that affect only males will not respond to natural selection, imposing a male-specific mitochondrial mutation load. Prior work has implicated this male-specific mutation load in disease and infertility, but new data from fruit flies suggests a prominent role for mtDNA in aging; across many taxa males almost invariably live shorter lives than females. Here we discuss this new work and identify some areas of future research that might now be encouraged to explore what may be the underpinning cause of the strong sexual dimorphism in aging.

摘要

线粒体功能是通过两个基因组的协同相互作用来实现的

一个是核基因组(nuDNA),另一个是线粒体基因组(mtDNA)。线粒体 DNA 的非典型传递方式主要是母系遗传而不发生重组,这被预测会影响雄性后代的适应度。最近的研究表明,衰老过程中的强烈性别二态性就是这种适应度后果之一。线粒体 DNA 的单亲遗传导致选择不对称性;只影响男性的突变不会受到自然选择的影响,从而产生男性特异性的线粒体突变负荷。先前的工作已经表明,这种男性特异性的突变负荷与疾病和不孕不育有关,但来自果蝇的新数据表明,线粒体 DNA 在衰老过程中起着重要作用;在许多分类群中,雄性的寿命几乎总是比雌性短。在这里,我们讨论这项新的工作,并确定一些未来研究的领域,这些领域现在可能会受到鼓励,以探索可能是衰老过程中强烈性别二态性的潜在根本原因。

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