Mapping H4K20me3 onto the chromatin landscape of senescent cells indicates a function in control of cell senescence and tumor suppression through preservation of genetic and epigenetic stability.

Histone modification H4K20me3 and its methyltransferase SUV420H2 have been implicated in suppression of tumorigenesis. The underlying mechanism is unclear, although abundance of H4K20me3 increases during cellular senescence. Cellular senescence is a stable proliferation arrest and tumor suppressor process, triggered by diverse molecular cues, including activated oncogenes. Here, we set out to better understand the function of H4K20me3 in senescence and tumor suppression. Overall design: ChIP-seq of H4K20me3 in RAS induced senescence and associated controls in IMR90 cells was performed. In total, four samples are included in the dataset which associates with a dataset that includes H4K20me3 ChIP in proliferating (PD32) and replicative senescent (PD87) samples.