Department of Biology, Carleton University, Ottawa, Ontario, Canada.
J Exp Zool B Mol Dev Evol. 2013 Jul;320(5):286-94. doi: 10.1002/jez.b.22499. Epub 2013 May 29.
There are two ways eukaryotes double number of chromosomes: (1) whole genome duplication (polyploidy), in which all nuclear DNA is replicated, and (2) karyotypic fission (pseudopolyploidy), in which all chromosomes are physically bifurcated. We contrast polyploidy with pseudopolyploidy, highlighting when it is crucial to look at genetic vs. genomic levels. We review history of pseudopolyploidy, including recent mechanisms by which chromosomal bifurcation may occur and outline methods for detecting such genomic changes. We then delve into the evolutionary implications, with particular focus on adaptive potential, of these two forms of doubling chromosome numbers. We address the common assertion that polyploidy induces adaptive radiations, which contains three fallacies. First, while polyploidy causes quantum speciation, evolutionary theory implies that these radiations should be non-adaptive. Polyploidy causes reproductive isolation, minute effective population sizes, and increased mutation rates, which all imply a diminished role for selection. Second, due to lack of karyotyping in recent decades and lack of distinction between genomic and genetic effects, it is usually impossible to detect pseudopolyploids. Third, pseudopolyploids lack minority cytotype exclusion because they readily backcross with their progenitors, which thereby means no reproductive isolation for newly formed pseudopolyploids. Pseudopolyploidy will thereby not result in radiations until pseudopolyploid descendants undergo subsequent chromosome rearrangements or grow new centromeres. Pseudopolyploids may have a modest selective advantage over their progenitors due to diminished linkage disequilibrium. Thus, pseudopolyploidy may induce adaptive non-radiations. We encourage a renaissance of karyotyping to distinguish between these two mechanisms and a renaissance in genomic perspectives in evolution.
(1) 全基因组复制(多倍体),即所有核 DNA 都被复制,(2) 染色体分裂(假多倍体),即所有染色体都发生物理分叉。我们对比了多倍体和假多倍体,强调了在查看遗传水平与基因组水平时的关键之处。我们回顾了假多倍体的历史,包括最近发生染色体分叉的机制,并概述了检测此类基因组变化的方法。然后,我们深入探讨了这两种染色体数量加倍形式的进化意义,特别关注其适应性潜力。我们解决了多倍体诱导适应性辐射这一常见说法中包含的三个谬论。首先,虽然多倍体导致量子种化,但进化理论意味着这些辐射应该是非适应性的。多倍体导致生殖隔离、微小的有效种群大小和增加的突变率,所有这些都意味着选择的作用减弱。其次,由于近几十年来缺乏染色体核型分析,以及缺乏对基因组和遗传效应的区分,通常无法检测到假多倍体。第三,假多倍体缺乏少数细胞型排斥,因为它们容易与祖先回交,从而为新形成的假多倍体提供了生殖隔离。只有当假多倍体后代经历随后的染色体重排或形成新的着丝粒时,假多倍体才会导致辐射,而不是立即导致辐射。假多倍体可能相对于其祖先具有适度的选择优势,因为它们的连锁不平衡减弱。因此,假多倍体可能会引起适应性的非辐射。我们鼓励重新进行染色体核型分析,以区分这两种机制,并重新关注进化中的基因组视角。