Ifg2-H19和Dlk1-Gtl2对小鼠孤雌生殖的双重屏障。

T Kono, M Kawahara, Q Wu, H Hiura, Y Obata
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引用次数: 6

摘要

母体和父系基因组之间的功能差异,其特征是配子体发生过程中的表观遗传修饰,即基因组印记,阻止了哺乳动物胚胎的孤雌生殖。基因组印迹导致来自母系和父系等位基因的印迹基因的不相等表达。然而,我们的研究表明,通过使用未生长的卵母细胞重建卵母细胞来改变母体印迹,同时删除H19基因,可以提供母体印迹基因的适当表达。在这里,我们讨论了在染色体7和12上父本印迹基因表达的进一步改变使ng/fg孤雌生殖胚胎发育到足月,这表明父本的贡献对后代是强制性的。
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Paternal dual barrier by Ifg2-H19 and Dlk1-Gtl2 to parthenogenesis in mice.

The functional difference between the maternal and paternal genome, which is characterized by epigenetic modifications during gametogenesis, that is genomic imprinting, prevents mammalian embryos from parthenogenesis. Genomic imprinting leads to nonequivalent expression of imprinted genes from the maternal and paternal alleles. However, our research showed that alteration of maternal imprinting by oocyte reconstruction using nongrowing oocytes together with deletion of the H19 gene, provides appropriate expression of maternally imprinted genes. Here we discuss that further alteration of paternally imprinted gene expressions at chromosomes 7 and 12 allows the ng/fg parthenogenetic embryos to develop to term, suggesting that the paternal contribution is obligatory for the descendant.

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