Imprinted X inactivation in eutherians: a model of gametic execution and zygotic relaxation
Imprinted X inactivation in eutherians: a model of gametic execution and zygotic relaxation
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DOI：
10.1016/s0955-0674(00)00272-6
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发表时间：
2001-12-01
影响因子：
7.5
通讯作者：
Lee, JT
中科院分区：
文献类型：
--
作者：
Huynh, KD;Lee, JT
在哺乳动物中，X染色体失活（XCl）通过转录沉默雌性细胞中的一条X染色体来确保XX和XY个体中X连锁基因的平等表达。在这篇综述中，我们讨论了一种印迹形式的X-失活，其中父亲的X（Xp）优先沉默。被认为是哺乳动物剂量补偿的祖先机制，印记X-失活仍然可以在现代有袋动物和一些真兽目动物（如小鼠）的胚外组织中观察到。最近的实验已经解决了配子印记的性质，并专注于非编码RNA基因Xist和其反义伴侣Tsix之间的相互作用。我们的文献回顾启发了一个非传统的看法，印迹XCl在小鼠中。首先，证据有力地表明，印记的Cl是不绝对的，因此随机数量的胚外细胞逃脱印记。第二，与传统的想法相反，我们想考虑这样一种可能性，即父亲的X染色体实际上可能作为一个预先失活的染色体传递给受精卵。在该模型中，配子启动并建立印迹XCl，而合子保持预先建立的配子失活模式。最后，我们假设，不绝对的性质是由不完善的合子维护印迹。我们建议，小鼠代表了一个过渡阶段的随机XCl从一个绝对的印记机制的演变。
In mammals, X-chromosome inactivation (XCl) ensures equal expression of X-linked genes in XX and XY individuals by transcriptionally silencing one X-chromosome in female cells. In this review, we discuss an imprinted form of X-inactivation in which the paternal X (Xp) is preferentially silenced. Believed to be the ancestral mechanism of dosage compensation in mammals, imprinted X-inactivation can still be observed in modern-day marsupials and in the extraembryonic tissues of some eutherians such as the mouse. Recent experiments have addressed the nature of the gametic imprint and focused on the regulatory interaction between the noncoding RNA gene, Xist, and its antisense partner, Tsix. Our review of the literature has inspired an unconventional view of imprinted XCl in mice. First, the evidence strongly argues that imprinted Cl is inabsolute, so that a stochastic number of extraembryonic cells escape imprinting. Second, contrary to conventional thinking, we would like to consider the possibility that the paternal X might actually be transmitted to the zygote as a pre-inactivated chromosome. In this model, the gamete initiates and establishes imprinted XCl, while the zygote maintains the pre-established pattern of gametic inactivation. Finally, we hypothesize that the inabsolute nature of imprinting is caused by imperfect zygotic maintenance. We propose that the mouse represents a transitional stage in the evolution of random XCl from an absolutely imprinted mechanism.