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Dissecting the precise role of H3K9 methylation in crosstalk with DNA maintenance methylation in mammals

Author

Listed:
  • Qian Zhao

    (Shanghai Key Laboratory of Regulatory Biology, The Institute of Biomedical Sciences and School of Life Sciences, East China Normal University)

  • Jiqin Zhang

    (Shanghai Key Laboratory of Regulatory Biology, The Institute of Biomedical Sciences and School of Life Sciences, East China Normal University)

  • Ruoyu Chen

    (Shanghai Key Laboratory of Regulatory Biology, The Institute of Biomedical Sciences and School of Life Sciences, East China Normal University)

  • Lina Wang

    (Shanghai Key Laboratory of Regulatory Biology, The Institute of Biomedical Sciences and School of Life Sciences, East China Normal University)

  • Bo Li

    (Shanghai Key Laboratory of Regulatory Biology, The Institute of Biomedical Sciences and School of Life Sciences, East China Normal University)

  • Hao Cheng

    (Key Laboratory of Computational Biology, CAS Center for Excellence in Molecular Cell Science, Collaborative Innovation Center for Genetics and Developmental Biology, Chinese Academy of Sciences-Max Planck Partner Institute for Computational Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences)

  • Xiaoya Duan

    (Shanghai Key Laboratory of Regulatory Biology, The Institute of Biomedical Sciences and School of Life Sciences, East China Normal University)

  • Haijun Zhu

    (Shanghai Key Laboratory of Regulatory Biology, The Institute of Biomedical Sciences and School of Life Sciences, East China Normal University)

  • Wei Wei

    (Shanghai Key Laboratory of Regulatory Biology, The Institute of Biomedical Sciences and School of Life Sciences, East China Normal University)

  • Jiwen Li

    (Shanghai Key Laboratory of Regulatory Biology, The Institute of Biomedical Sciences and School of Life Sciences, East China Normal University)

  • Qihan Wu

    (Shanghai Key Laboratory of Regulatory Biology, The Institute of Biomedical Sciences and School of Life Sciences, East China Normal University)

  • Jing-Dong J. Han

    (Key Laboratory of Computational Biology, CAS Center for Excellence in Molecular Cell Science, Collaborative Innovation Center for Genetics and Developmental Biology, Chinese Academy of Sciences-Max Planck Partner Institute for Computational Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences)

  • Wenqiang Yu

    (Laboratory of RNA Epigenetics, Institutes of Biomedical Sciences, Shanghai Medical College, Fudan University)

  • Shaorong Gao

    (Clinical and Translational Research Center of Shanghai First Maternity, Infant Hospital, School of Life Sciences and Technology, Tongji University)

  • Guohong Li

    (National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences)

  • Jiemin Wong

    (Shanghai Key Laboratory of Regulatory Biology, The Institute of Biomedical Sciences and School of Life Sciences, East China Normal University
    Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center)

Abstract

In mammals it is unclear if UHRF1-mediated DNA maintenance methylation by DNMT1 is strictly dependent on histone H3K9 methylation. Here we have generated an Uhrf1 knockin (KI) mouse model that specifically abolishes the H3K9me2/3-binding activity of Uhrf1. The homozygous Uhrf1 KI mice are viable and fertile, and exhibit ∼10% reduction of DNA methylation in various tissues. The reduced DNA methylation occurs globally in the genome and does not restrict only to the H3K9me2/3 enriched repetitive sequences. In vitro UHRF1 binds with higher affinity to reconstituted nucleosome with hemi-methylated CpGs than that with H3K9me2/3, although it binds cooperatively to nucleosome with both modifications. We also show that the nucleosome positioning affects the binding of methylated DNA by UHRF1. Thus, while our study supports a role for H3K9 methylation in promoting DNA methylation, it demonstrates for the first time that DNA maintenance methylation in mammals is largely independent of H3K9 methylation.

Suggested Citation

  • Qian Zhao & Jiqin Zhang & Ruoyu Chen & Lina Wang & Bo Li & Hao Cheng & Xiaoya Duan & Haijun Zhu & Wei Wei & Jiwen Li & Qihan Wu & Jing-Dong J. Han & Wenqiang Yu & Shaorong Gao & Guohong Li & Jiemin Wo, 2016. "Dissecting the precise role of H3K9 methylation in crosstalk with DNA maintenance methylation in mammals," Nature Communications, Nature, vol. 7(1), pages 1-12, November.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12464
    DOI: 10.1038/ncomms12464
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    Cited by:

    1. Zeyang Wang & Rui Fan & Angela Russo & Filippo M. Cernilogar & Alexander Nuber & Silvia Schirge & Irina Shcherbakova & Iva Dzhilyanova & Enes Ugur & Tobias Anton & Lisa Richter & Heinrich Leonhardt & , 2022. "Dominant role of DNA methylation over H3K9me3 for IAP silencing in endoderm," Nature Communications, Nature, vol. 13(1), pages 1-14, December.

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