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Histone variant H2A.J accumulates in senescent cells and promotes inflammatory gene expression

Author

Listed:
  • Kévin Contrepois

    (Institute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Univ. Paris-Sud, Université Paris-Saclay
    Stanford University)

  • Clément Coudereau

    (Institute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Univ. Paris-Sud, Université Paris-Saclay)

  • Bérénice A. Benayoun

    (Stanford University
    Paul F. Glenn Laboratories for the Biology of Aging, Stanford University, Stanford, California 94305-5120, USA)

  • Nadine Schuler

    (Saarland University)

  • Pierre-François Roux

    (Institut Pasteur/INSERM U933, Laboratory of Nuclear Organization and Oncogenesis)

  • Oliver Bischof

    (Institut Pasteur/INSERM U933, Laboratory of Nuclear Organization and Oncogenesis)

  • Régis Courbeyrette

    (Institute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Univ. Paris-Sud, Université Paris-Saclay)

  • Cyril Carvalho

    (Institute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Univ. Paris-Sud, Université Paris-Saclay)

  • Jean-Yves Thuret

    (Institute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Univ. Paris-Sud, Université Paris-Saclay)

  • Zhihai Ma

    (Stanford University)

  • Céline Derbois

    (CEA, CNG)

  • Marie-Claire Nevers

    (CEA, Service de Pharmacologie et Immunoanalyse (SPI), INRA, Université Paris-Saclay)

  • Hervé Volland

    (CEA, Service de Pharmacologie et Immunoanalyse (SPI), INRA, Université Paris-Saclay)

  • Christophe E. Redon

    (Laboratory of Molecular Pharmacology, C.C.R., N.C.I., N.I.H.)

  • William M. Bonner

    (Laboratory of Molecular Pharmacology, C.C.R., N.C.I., N.I.H.)

  • Jean-François Deleuze

    (CEA, CNG)

  • Clotilde Wiel

    (Inserm U1052, Centre de Recherche en Cancérologie de Lyon, CNRS UMR5286, Centre Léon Bérard, Université de Lyon)

  • David Bernard

    (Inserm U1052, Centre de Recherche en Cancérologie de Lyon, CNRS UMR5286, Centre Léon Bérard, Université de Lyon)

  • Michael P. Snyder

    (Stanford University)

  • Claudia E. Rübe

    (Saarland University)

  • Robert Olaso

    (CEA, CNG)

  • François Fenaille

    (CEA, IBITECS, Service de Pharmacologie et d'Immunoanalyse, UMR 0496, Laboratoire d'Etude du Métabolisme des Médicaments, MetaboHUB-Paris, Université Paris Saclay)

  • Carl Mann

    (Institute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Univ. Paris-Sud, Université Paris-Saclay)

Abstract

The senescence of mammalian cells is characterized by a proliferative arrest in response to stress and the expression of an inflammatory phenotype. Here we show that histone H2A.J, a poorly studied H2A variant found only in mammals, accumulates in human fibroblasts in senescence with persistent DNA damage. H2A.J also accumulates in mice with aging in a tissue-specific manner and in human skin. Knock-down of H2A.J inhibits the expression of inflammatory genes that contribute to the senescent-associated secretory phenotype (SASP), and over expression of H2A.J increases the expression of some of these genes in proliferating cells. H2A.J accumulation may thus promote the signalling of senescent cells to the immune system, and it may contribute to chronic inflammation and the development of aging-associated diseases.

Suggested Citation

  • Kévin Contrepois & Clément Coudereau & Bérénice A. Benayoun & Nadine Schuler & Pierre-François Roux & Oliver Bischof & Régis Courbeyrette & Cyril Carvalho & Jean-Yves Thuret & Zhihai Ma & Céline Derbo, 2017. "Histone variant H2A.J accumulates in senescent cells and promotes inflammatory gene expression," Nature Communications, Nature, vol. 8(1), pages 1-18, August.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14995
    DOI: 10.1038/ncomms14995
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