It is almost ten years since senescence associated heterochromatic foci (SAHFs) 
were first described in human diploid fibroblasts (HDFs). Since then, a number 
of factors have been identified that affect SAHF formation, including HMGA 
proteins, structural components of SAHFs. However, the involvement of epigenetic 
marks in SAHF formation remains unclear. Our recent study, combining microscopy 
and ChIP-seq approaches, revealed that SAHFs are formed through spatial 
repositioning of the genome. This occurs according to certain chromatin features 
that are correlated with, but do not require, the repressive marks histone H3 
trimethylated on lysine 9 (H3K9me3) and H3K27me3. These repressive marks are 
segregated from each other within SAHFs, forming layered high-order chromatin 
structures (HOCS). During the dynamic change in HOCS as SAHFs form, the linear 
epigenomic profiles of these repressive marks are highly static. This is in 
marked contrast to the spreading of repressive marks occurring during embryonic 
cell differentiation. Thus the layered HOCS of SAHFs is likely achieved mainly 
through the spatial rearrangement of pre-existing heterochromatin, rather than 
spreading of heterochromatin. Evidence for the co-association of similar types 
of chromatin is emerging and SAHFs may provide a unique model system to study 
the correlation between HOCS and chromatin types, which are readily visible and 
regulable.