期刊
NATURE COMMUNICATIONS
卷 8, 期 -, 页码 -出版社
NATURE PORTFOLIO
DOI: 10.1038/ncomms14995
关键词
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资金
- Fondation pour la Recherche Medicale [DEP20131128527]
- Association pour la Recherche sur le Cancer
- Comite de l'Essonne de la Ligue Contre le Cancer
- CEA Plasticity and Instability of the Genome Program
- ARC foundation
- Dean's fellowship at Stanford University
- NIA [K99 AG049934]
- German Research Foundation [RU 821/3-1]
- European Atomic Energy Community's Seventh Framework Programme [249689]
- NIH [5P01GM09913005, 5P50HG00773502]
- Center for Cancer Research, National Cancer Institute, National Institutes of Health
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.
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