Transposable elements are regulated by context-specific patterns of chromatin marks in mouse embryonic stem cells
Jiangping He,
Xiuling Fu,
Meng Zhang,
Fangfang He,
Wenjuan Li,
Mazid Md. Abdul,
Jianguo Zhou,
Li Sun,
Chen Chang,
Yuhao Li,
He Liu,
Kaixin Wu,
Isaac A. Babarinde,
Qiang Zhuang,
Yuin-Han Loh,
Jiekai Chen,
Miguel A. Esteban and
Andrew P. Hutchins ()
Additional contact information
Jiangping He: Chinese Academy of Sciences
Xiuling Fu: Southern University of Science and Technology
Meng Zhang: Chinese Academy of Sciences
Fangfang He: Southern University of Science and Technology
Wenjuan Li: Chinese Academy of Sciences
Mazid Md. Abdul: Chinese Academy of Sciences
Jianguo Zhou: Chinese Academy of Sciences
Li Sun: Southern University of Science and Technology
Chen Chang: Southern University of Science and Technology
Yuhao Li: Southern University of Science and Technology
He Liu: Chinese Academy of Sciences
Kaixin Wu: Chinese Academy of Sciences
Isaac A. Babarinde: Southern University of Science and Technology
Qiang Zhuang: Southern University of Science and Technology
Yuin-Han Loh: A*STAR Institute of Molecular and Cell Biology
Jiekai Chen: Chinese Academy of Sciences
Miguel A. Esteban: Chinese Academy of Sciences
Andrew P. Hutchins: Southern University of Science and Technology
Nature Communications, 2019, vol. 10, issue 1, 1-13
Abstract:
Abstract The majority of mammalian genomes are devoted to transposable elements (TEs). Whilst TEs are increasingly recognized for their important biological functions, they are a potential danger to genomic stability and are carefully regulated by the epigenetic system. However, the full complexity of this regulatory system is not understood. Here, using mouse embryonic stem cells, we show that TEs are suppressed by heterochromatic marks like H3K9me3, and are also labelled by all major types of chromatin modification in complex patterns, including bivalent activatory and repressive marks. We identified 29 epigenetic modifiers that significantly deregulated at least one type of TE. The loss of Setdb1, Ncor2, Rnf2, Kat5, Prmt5, Uhrf1, and Rrp8 caused widespread changes in TE expression and chromatin accessibility. These effects were context-specific, with different chromatin modifiers regulating the expression and chromatin accessibility of specific subsets of TEs. Our work reveals the complex patterns of epigenetic regulation of TEs.
Date: 2019
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DOI: 10.1038/s41467-018-08006-y
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