Undermethylation associated with retroelement activation and chromosome remodelling in an interspecific mammalian hybrid
Undermethylation associated with retroelement activation and chromosome remodelling in an interspecific mammalian hybrid
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DOI：
10.1038/29985
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发表时间：
1998-05-07
期刊：
影响因子：
64.8
通讯作者：
Graves, JAM
中科院分区：
文献类型：
--
作者：
O'Neill, RJW;O'Neill, MJ;Graves, JAM
遗传模型(1，2)预测，杂交种的基因组重排可以通过阻止亲本物种和杂交种之间的基因流动来促进生殖隔离和新物种的形成(向日葵是一个例子(3))。杂交诱导染色体重塑的机制尚不清楚，尽管在一些发育不良的果蝇杂交中，可移动元件的活性被证明与DNA重排有关(4，5)，但已提出DNA甲基化是作为一种抑制可移动元件运动的手段进化的(宿主防御模型(6，7))。如果这种保护机制失效，可移动元件可能被激活，并可能导致重大和快速的基因组改变(8，9)，在这里，我们证明了在种间杂交哺乳动物(Macropus Eugenii X Wallabia Biolor)中发生了全基因组甲基化不足、逆转录病毒元件扩增和染色体重塑。杂交后代中常染色体的非典型延伸着丝粒主要由一种未甲基化的、扩增的逆转录病毒元件组成，在两个亲本物种中都检测不到。这些结果与其他哺乳动物杂交种的甲基化缺陷和从头染色体变化的观察相结合，表明杂交种中DNA甲基化的失败和随后的可移动元件活性可能有助于核型的快速进化。
Genetic models(1,2) predict that genomic rearrangement in hybrids can facilitate reproductive isolation and the formation of new species by preventing gene flow between the parent species and hybrid (sunflowers are an example(3)). The mechanism underlying hybridization-induced chromosome remodelling is as yet unknown, although mobile element activity has been shown to be involved in DNA rearrangement in some dysgenic Drosophila hybrids(4,5), It has been proposed that DNA methylation evolved as a means of repressing the movement of mobile elements (the host defence model(6,7)). If such a protective mechanism were to fail, mobile elements could be activated, and could cause major and rapid genome alterations(8,9), Here we demonstrate the occurrence of genome-wide undermethylation, retroviral element amplification and chromosome remodelling in an interspecific mammalian hybrid (Macropus eugenii X Wallabia bicolor). Atypically extended centromeres of Macropus eugenii derived autosomes in the hybrid were composed primarily of an unmethylated, amplified retroviral element not detectable in either parent species. These results, taken with the observation of deficient methylation and de novo chromosome change in other mammalian hybrids, indicate that the failure of DNA methylation and subsequent mobile-element activity in hybrids could facilitate rapid karyotypic evolution.