Deletion of Peg10, an imprinted gene acquired from a retrotransposon, causes early embryonic lethality
Deletion of Peg10, an imprinted gene acquired from a retrotransposon, causes early embryonic lethality
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DOI：
10.1038/ng1699
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发表时间：
2006-01-01
期刊：
影响因子：
30.8
通讯作者：
Ishino, F
中科院分区：
文献类型：
--
作者：
Ono, R;Nakamura, K;Ishino, F
通过比较哺乳动物基因组，我们和其他人已经鉴定了具有高度保守的DNA序列和插入位点的活跃转录的Ty 3/gypsy逆转录转座子衍生基因（1-6）。为了阐明哺乳动物发育中进化上保守的逆转录转座子衍生基因的功能，我们产生了缺乏这些基因之一的小鼠，Peg 10（父系表达10）（1- 3，7），其是小鼠近端染色体6上的父系表达印迹基因。由于胎盘缺陷，Peg 10基因敲除小鼠显示出早期胚胎死亡。这表明Peg 10对小鼠孤雌发育至关重要，并提供了进化上保守的逆转录转座子衍生基因在哺乳动物发育中的重要作用的第一个直接证据。
By comparing mammalian genomes, we and others have identified actively transcribed Ty3/gypsy retrotransposon-derived genes with highly conserved DNA sequences and insertion sites(1-6). To elucidate the functions of evolutionarily conserved retrotransposon-derived genes in mammalian development, we produced mice that lack one of these genes, Peg10 ( paternally expressed 10)(1-3,7), which is a paternally expressed imprinted gene on mouse proximal chromosome 6. The Peg10 knockout mice showed early embryonic lethality owing to defects in the placenta. This indicates that Peg10 is critical for mouse parthenogenetic development and provides the first direct evidence of an essential role of an evolutionarily conserved retrotransposon-derived gene in mammalian development.