Role of retrotransposon-derived imprinted gene, Rtl1, in the feto-maternal interface of mouse placenta
Role of retrotransposon-derived imprinted gene, Rtl1, in the feto-maternal interface of mouse placenta
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DOI：
10.1038/ng.2007.51
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发表时间：
2008-02-01
期刊：
影响因子：
30.8
通讯作者：
Ishino, Fumitoshi
中科院分区：
文献类型：
--
作者：
Sekita, Yoichi;Wagatsuma, Hirotaka;Ishino, Fumitoshi
真兽胎盘是哺乳动物进化过程中出现的一种器官，通过在胎儿和母体血液之间交换营养、气体和废物，为胎儿发育提供必要的结构，即所谓的胎儿-母体界面。胎盘的功能缺陷会导致几种发育障碍，如人类和小鼠的宫内发育迟缓。一系列新的发明和/或适应必须形成和维持真兽绒毛尿囊胎盘，其由毛细血管内皮细胞和周围的滋养层细胞层组成（1）。虽然许多胎盘基因已被鉴定（2），但仍不清楚胎儿-母体界面在发育过程中如何形成和维持，以及这种新设计如何进化。在这里，我们证明，逆转录转座子衍生的Rtl 1（逆转录转座子样1），也被称为Peg 11（父系表达11），是必不可少的胎儿毛细血管的维护，它的损失和过度生产造成晚期胎儿和/或新生儿致死小鼠。
Eutherian placenta, an organ that emerged in the course of mammalian evolution, provides essential architecture, the so-called feto-maternal interface, for fetal development by exchanging nutrition, gas and waste between fetal and maternal blood. Functional defects of the placenta cause several developmental disorders, such as intrauterine growth retardation in humans and mice. A series of new inventions and/ or adaptations must have been necessary to form and maintain eutherian chorioallantoic placenta, which consists of capillary endothelial cells and a surrounding trophoblast cell layer(s)(1). Although many placental genes have been identified(2), it remains unknown how the feto-maternal interface is formed and maintained during development, and how this novel design evolved. Here we demonstrate that retrotransposon-derived Rtl1 (retrotransposon-like 1), also known as Peg11 (paternally expressed 11), is essential for maintenance of the fetal capillaries, and that both its loss and its overproduction cause late-fetal and/or neonatal lethality in mice.