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

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. Overall design: 41 samples analysed