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核-线粒体上位性:从基因视角看基因组冲突。

Nuclear-mitochondrial epistasis: a gene's eye view of genomic conflict.

作者信息

Wade Michael J, Drown Devin M

机构信息

Department of Biology Indiana University Bloomington Indiana 47405.

Department of Biology Indiana University Bloomington Indiana 47405; Institute of Arctic Biology University of Alaska Fairbanks Fairbanks Alaska 99775.

出版信息

Ecol Evol. 2016 Aug 18;6(18):6460-6472. doi: 10.1002/ece3.2345. eCollection 2016 Sep.

DOI:10.1002/ece3.2345
PMID:27777722
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5058520/
Abstract

We use population genetic models to investigate the cooperative and conflicting synergistic fitness effects between genes from the nucleus and the mitochondrion. By varying fitness parameters, we examine the scope for conflict relative to cooperation among genomes and the utility of the "gene's eye view" analytical approach, which is based on the marginal average fitness of specific alleles. Because sexual conflict can maintain polymorphism of mitochondrial haplotypes, we can explore two types of evolutionary conflict (genomic and sexual) with one epistatic model. We find that the nuclear genetic architecture (autosomal, X-linked, or Z-linked) and the mating system change the regions of parameter space corresponding to the evolution by sexual and genomic conflict. For all models, regardless of conflict or cooperation, we find that population mean fitness increases monotonically as evolution proceeds. Moreover, we find that the process of gene frequency change with positive, synergistic fitnesses is self-accelerating, as the success of an allele in one genome or in one sex increases the frequency of the interacting allele upon which its success depends. This results in runaway evolutionary dynamics caused by the positive intergenomic associations generated by selection. An inbreeding mating system tends to further accelerate these runaway dynamics because it maintains favorable host-symbiont or male-female gene combinations. In contrast, where conflict predominates, the success of an allele in one genome or in one sex diminishes the frequency of the corresponding allele in the other, resulting in considerably slower evolutionary dynamics. The rate of change of mean fitness is also much faster with positive, synergistic fitnesses and much slower where conflict is predominant. Consequently, selection rapidly fixes cooperative gene combinations, while leaving behind a slowing evolving residue of conflicting gene combinations at mutation-selection balance. We discuss how an emphasis on marginal fitness averages may obscure the interdependence of allelic fitness across genomes, making the evolutionary trajectories appear independent of one another when they are not.

摘要

我们使用群体遗传模型来研究细胞核基因与线粒体基因之间协同的、相互冲突的协同适应度效应。通过改变适应度参数,我们检验相对于基因组间合作而言冲突的范围,以及基于特定等位基因边际平均适应度的“基因视角”分析方法的效用。由于性冲突可维持线粒体单倍型的多态性,我们能够用一个上位性模型来探究两种类型的进化冲突(基因组冲突和性冲突)。我们发现核遗传结构(常染色体、X连锁或Z连锁)以及交配系统会改变与性冲突和基因组冲突进化相对应的参数空间区域。对于所有模型,无论冲突或合作情况如何,我们发现随着进化的进行,群体平均适应度单调增加。此外,我们发现当适应度为正且具有协同性时,基因频率变化过程是自我加速的,因为一个等位基因在一个基因组或一种性别中的成功会增加其成功所依赖的相互作用等位基因的频率。这导致了由选择产生的正基因组间关联所引起的失控进化动态。近交交配系统往往会进一步加速这些失控动态,因为它维持了有利的宿主 - 共生体或雌雄基因组合。相比之下,在冲突占主导的情况下,一个等位基因在一个基因组或一种性别中的成功会降低另一个基因组或性别的相应等位基因的频率,导致进化动态显著变慢。当适应度为正且具有协同性时,平均适应度的变化速率也快得多,而在冲突占主导时则慢得多。因此,选择会迅速固定协同的基因组合,同时在突变 - 选择平衡状态下留下进化缓慢的冲突基因组合残余。我们讨论了对边际适应度平均值的强调可能如何掩盖基因组间等位基因适应度的相互依赖性,使得进化轨迹在实际上并非相互独立时却显得彼此独立。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227b/5058520/132d837de210/ECE3-6-6460-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227b/5058520/9628e5d11a3b/ECE3-6-6460-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227b/5058520/cc0cae39e803/ECE3-6-6460-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227b/5058520/d1d6005bffd9/ECE3-6-6460-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227b/5058520/8459fae84880/ECE3-6-6460-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227b/5058520/b601e9112992/ECE3-6-6460-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227b/5058520/132d837de210/ECE3-6-6460-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227b/5058520/9628e5d11a3b/ECE3-6-6460-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227b/5058520/cc0cae39e803/ECE3-6-6460-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227b/5058520/d1d6005bffd9/ECE3-6-6460-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227b/5058520/8459fae84880/ECE3-6-6460-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227b/5058520/b601e9112992/ECE3-6-6460-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/227b/5058520/132d837de210/ECE3-6-6460-g006.jpg

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