Genomic imprinting defect in Zfp57 mutant iPS cell lines.
Genomic imprinting defect in Zfp57 mutant iPS cell lines.
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DOI：
10.1016/j.scr.2016.01.018
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发表时间：
2016-03
影响因子：
1.2
通讯作者：
Li X
中科院分区：
文献类型：
--
作者：
McDonald CM;Liu L;Xiao L;Schaniel C;Li X
ZFP 57在小鼠胚胎和ES细胞中维持基因组印记。为了测试其在iPS重编程过程中的作用，我们通过利用逆转录病毒感染在小鼠MEF细胞中表达重编程因子来获得iPS克隆。在分析了4个印迹区域后，我们发现双亲来源的DNA甲基化印迹在含有Zfp 57的iPS克隆中大部分得以保留，而在没有母本或合子Zfp 57的iPS克隆中缺失。有趣的是，在没有合子Zfp 57的iPS克隆中，DNA甲基化印记在Peg 1和Peg 3处丢失，但保留在Snrpn和Dlk 1-Dio 3印记区域。这一发现将在未来的研究中继续进行。
ZFP57 maintains genomic imprinting in mouse embryos and ES cells. To test its roles during iPS reprogamming, we derived iPS clones by utilizing retroviral infection to express reprogramming factors in mouse MEF cells. After analyzing four imprinted regions, we found parentally derived DNA methylation imprint was largely maintained in the iPS clones with Zfp57 but missing in those without maternal or zygotic Zfp57. Intriguingly, DNA methylation imprint was lost at the Peg1 and Peg3 but retained at the Snrpn and Dlk1-Dio3 imprinted regions in the iPS clones without zygotic Zfp57. This finding will be pursued in future studies.