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Evolutionary epigenomic analyses in mammalian early embryos reveal species-specific innovations and conserved principles of imprinting

文献类型： 外文期刊

作者： Lu, Xukun 1 ; Zhang, Yu 1 ; Wang, Lijuan 2 ; Wang, Leyun 4 ; Wang, Huili 6 ; Xu, Qianhua 1 ; Xiang, Yunlong 1 ; Chen, Cha 1 ;

作者机构： 1.Tsinghua Peking Ctr Life Sci, Beijing 100084, Peoples R China

2.Tsinghua Univ, Ctr Stem Cell Biol & Regenerat Med, Sch Life Sci, MOE Key Lab Bioinformat, Beijing 100084, Peoples R China

3.Beijing Univ Agr, Coll Anim Sci & Technol, Beijing 102206, Peoples R China

4.Chinese Acad Sci, Inst Zool, State Key Lab Stem Cell & Reprod Biol, Beijing 100101, Peoples R China

5.Chinese Acad Sci, Inst Stem Cell & Regenerat, Beijing 100101, Peoples R China

6.Jiangsu Acad Agr Sci, Inst Anim Sci, Nanjing 210014, Peoples R China

7.Northeast Agr Univ, Coll Life Sci, Harbin 150030, Peoples R China

期刊名称：SCIENCE ADVANCES （ 影响因子：14.143； 五年影响因子：16.45 ）

ISSN： 2375-2548

年卷期： 2021 年 7 卷 48 期

页码：

收录情况： SCI

摘要： While mouse remains the most popular model, the conservation of parental-to-embryonic epigenetic transition across mammals is poorly defined. Through analysis of oocytes and early embryos in human, bovine, porcine, rat, and mouse, we revealed remarkable species-specific innovations as no single animal model fully recapitulates the human epigenetic transition. In rodent oocytes, transcription-dependent DNA methylation allows methylation of maternal imprints but not intergenic paternal imprints. Unexpectedly, prevalent DNA hypermethylation, paralleled by H3K36me2/3, also occurs in nontranscribed regions in porcine and bovine oocytes, except for megabase--long "CpG continents (CGCs)" where imprinting control regions preferentially reside. Broad H3K4me3 and H3K27me3 domains exist in nonhuman oocytes, yet only rodent H3K27me3 survives beyond genome activation. Coincidently, regulatory elements preferentially evade H3K27me3 in rodent oocytes, and failure to do so causes aberrant embryonic gene repression. Hence, the diverse mammalian innovations of parental-to-embryonic transition center on a delicate "to-methylate-or-not" balance in establishing imprints while protecting other regulatory regions.

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