Resetting histone modifications during human parental-to-zygotic transition

Weikun Xia(Center for Life Sciences), Jiawei Xu(First Affiliated Hospital of Zhengzhou University), Guang Yu(Center for Life Sciences), Guidong Yao(First Affiliated Hospital of Zhengzhou University), Kai Xu(Center for Life Sciences), Xue‐Shan Ma(First Affiliated Hospital of Zhengzhou University), Nan Zhang(First Affiliated Hospital of Zhengzhou University), Bofeng Liu(Center for Life Sciences), Tong Li(First Affiliated Hospital of Zhengzhou University), Zili Lin(Center for Life Sciences), Xia Chen(Tsinghua University), Lijia Li(Center for Life Sciences), Q. Wang(Center for Life Sciences), Dayuan Shi(First Affiliated Hospital of Zhengzhou University), Senlin Shi(First Affiliated Hospital of Zhengzhou University), Yile Zhang(First Affiliated Hospital of Zhengzhou University), Wenyan Song(First Affiliated Hospital of Zhengzhou University), Haixia Jin(First Affiliated Hospital of Zhengzhou University), Linli Hu(First Affiliated Hospital of Zhengzhou University), Zhiqin Bu(First Affiliated Hospital of Zhengzhou University), Yang Wang(First Affiliated Hospital of Zhengzhou University), Jie Na(Tsinghua University), Wei Xie(Center for Life Sciences), Ying-Pu Sun(First Affiliated Hospital of Zhengzhou University)
Science
July 4, 2019
Cited by 277Open Access
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Abstract

Histone modifications regulate gene expression and development. To address how they are reprogrammed in human early development, we investigated key histone marks in human oocytes and early embryos. Unlike that in mouse oocytes, the permissive mark trimethylated histone H3 lysine 4 (H3K4me3) largely exhibits canonical patterns at promoters in human oocytes. After fertilization, prezygotic genome activation (pre-ZGA) embryos acquire permissive chromatin and widespread H3K4me3 in CpG-rich regulatory regions. By contrast, the repressive mark H3K27me3 undergoes global depletion. CpG-rich regulatory regions then resolve to either active or repressed states upon ZGA, followed by subsequent restoration of H3K27me3 at developmental genes. Finally, by combining chromatin and transcriptome maps, we revealed transcription circuitry and asymmetric H3K27me3 patterning during early lineage specification. Collectively, our data unveil a priming phase connecting human parental-to-zygotic epigenetic transition.


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