Cellular senescence involves chromatin remodelling, and Ivanov et al. show here that an autophagy–lysosome pathway contributes to this. They observed more cytoplasmic chromatin fragments (CCFs) in senescent cells than in proliferating cells; these were positive for the DNA damage marker γH2A.X and the heterochromatic histone mark H3K27me3 (trimethylated Lys27 of histone H3). Using time-lapse imaging they observed that CCFs associated with these marks entered the cytoplasm by 'blebbing' off the cell nucleus and that the integrity of the nuclear envelope was compromised in senescent cells. The authors also found that CCFs partially colocalize with autophagy markers and that the level of a lysosomal protease (cathepsin L) that cleaves histone H3 to produce histone H3cs1 was increased in senescent cells, along with H3cs1 levels. The histone content of senescent cells was also reduced in a lysosome-dependent manner. The authors conclude that “autophagy and lysosomes contribute to the proteolytic processing of histones in senescence.”