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Chromatin decompaction by the nucleosomal binding protein HMGN5 impairs nuclear sturdiness

Author

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  • Takashi Furusawa

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

  • Mark Rochman

    (Protein Section, Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health
    Present address: Division of Allergy and Immunology, Cincinnati Children’s Hospital, Cincinnati, Ohio 45229, USA)

  • Leila Taher

    (Institute for Biostatistics and Informatics in Medicine and Ageing Research, University of Rostock)

  • Emilios K. Dimitriadis

    (Biomedical Engineering and Physical Science Shared Resource Program, National Institute of Biomedical Imaging and Bioengineering, National Institutes of Health)

  • Kunio Nagashima

    (Electron microscopy laboratory, Leidos Biomedical Research Inc., SAIC-Frederick Inc.,Frederick National Laboratory for Cancer Research)

  • Stasia Anderson

    (Animal Core Facility, National Heart Lung and Blood Institute, National Institutes of Health)

  • Michael Bustin

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

Abstract

In most metazoan nuclei, heterochromatin is located at the nuclear periphery in contact with the nuclear lamina, which provides mechanical stability to the nucleus. We show that in cultured cells, chromatin decompaction by the nucleosome binding protein HMGN5 decreases the sturdiness, elasticity and rigidity of the nucleus. Mice overexpressing HMGN5, either globally or only in the heart, are normal at birth but develop hypertrophic heart with large cardiomyoctyes, deformed nuclei and disrupted lamina and die of cardiac malfunction. Chromatin decompaction is seen in cardiomyocytes of newborn mice but misshaped nuclei with disrupted lamina are seen only in adult cardiomyocytes, suggesting that loss of heterochromatin diminishes the ability of the nucleus to withstand the mechanical forces of the contracting heart. Thus, heterochromatin enhances the ability of the nuclear lamina to maintain the sturdiness and shape of the eukaryotic nucleus; a structural role for chromatin that is distinct from its genetic functions.

Suggested Citation

  • Takashi Furusawa & Mark Rochman & Leila Taher & Emilios K. Dimitriadis & Kunio Nagashima & Stasia Anderson & Michael Bustin, 2015. "Chromatin decompaction by the nucleosomal binding protein HMGN5 impairs nuclear sturdiness," Nature Communications, Nature, vol. 6(1), pages 1-10, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7138
    DOI: 10.1038/ncomms7138
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