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Binding of HMGN proteins to cell specific enhancers stabilizes cell identity

Author

Listed:
  • Bing He

    (Protein Section, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health)

  • Tao Deng

    (Protein Section, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health)

  • Iris Zhu

    (Computational Biology Branch, National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health)

  • Takashi Furusawa

    (Protein Section, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health)

  • Shaofei Zhang

    (Protein Section, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health)

  • Wei Tang

    (Laboratory of Human Carcinogenesis, Center for Cancer Research, National Institutes of Health)

  • Yuri Postnikov

    (Protein Section, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health)

  • Stefan Ambs

    (Laboratory of Human Carcinogenesis, Center for Cancer Research, National Institutes of Health)

  • Caiyi Cherry Li

    (Laboratory of Genomic Integrity, Center for Cancer Research National Cancer Institute National Institutes of Health)

  • Ferenc Livak

    (Laboratory of Genomic Integrity, Center for Cancer Research National Cancer Institute National Institutes of Health)

  • David Landsman

    (Computational Biology Branch, National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health)

  • Michael Bustin

    (Protein Section, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health)

Abstract

The dynamic nature of the chromatin epigenetic landscape plays a key role in the establishment and maintenance of cell identity, yet the factors that affect the dynamics of the epigenome are not fully known. Here we find that the ubiquitous nucleosome binding proteins HMGN1 and HMGN2 preferentially colocalize with epigenetic marks of active chromatin, and with cell-type specific enhancers. Loss of HMGNs enhances the rate of OSKM induced reprogramming of mouse embryonic fibroblasts (MEFs) into induced pluripotent stem cells (iPSCs), and the ASCL1 induced conversion of fibroblast into neurons. During transcription factor induced reprogramming to pluripotency, loss of HMGNs accelerates the erasure of the MEF-specific epigenetic landscape and the establishment of an iPSCs-specific chromatin landscape, without affecting the pluripotency potential and the differentiation potential of the reprogrammed cells. Thus, HMGN proteins modulate the plasticity of the chromatin epigenetic landscape thereby stabilizing, rather than determining cell identity.

Suggested Citation

  • Bing He & Tao Deng & Iris Zhu & Takashi Furusawa & Shaofei Zhang & Wei Tang & Yuri Postnikov & Stefan Ambs & Caiyi Cherry Li & Ferenc Livak & David Landsman & Michael Bustin, 2018. "Binding of HMGN proteins to cell specific enhancers stabilizes cell identity," Nature Communications, Nature, vol. 9(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-07687-9
    DOI: 10.1038/s41467-018-07687-9
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    Cited by:

    1. Ravikanth Nanduri & Takashi Furusawa & Alexei Lobanov & Bing He & Carol Xie & Kimia Dadkhah & Michael C. Kelly & Oksana Gavrilova & Frank J. Gonzalez & Michael Bustin, 2022. "Epigenetic regulation of white adipose tissue plasticity and energy metabolism by nucleosome binding HMGN proteins," Nature Communications, Nature, vol. 13(1), pages 1-15, December.
    2. Dmitry A. Kretov & Leighton Folkes & Alexandra Mora-Martin & Isha A. Walawalkar & Imrat & Noreen Syedah & Kim Vanuytsel & Simon Moxon & George J. Murphy & Daniel Cifuentes, 2024. "The miR-144/Hmgn2 regulatory axis orchestrates chromatin organization during erythropoiesis," Nature Communications, Nature, vol. 15(1), pages 1-15, December.

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