A novel histone variant H2A.J accumulates in senescent human cell with persistent DNA damage and promote inflammatory gene expression

The senescence of mammalian cells is characterized by a proliferative arrest in response to stress and the expression of an inflammatory phenotype. We discovered that H2A.J, a poorly studied H2A variant found only in mammals, accumulates in human fibroblasts in senescence with persistent DNA damage. Knock-down of H2A.J interfered with the derepression of a set of inflammatory genes that contribute to the senescent-associated secretory phenotype (SASP), and over-expression of H2A.J increased the expression of some of these genes in proliferating cells. H2A.J accumulation may thus promote the signaling of senescent cells to the immune system. 41 samples analysed