In genetics and epigenetics, bookmarking is a biological phenomenon believed to function as an epigenetic mechanism for transmitting cellular memory of the pattern of gene expression in a cell, throughout mitosis, to its daughter cells. This is vital for maintaining the phenotype in a lineage of cells so that, for example, liver cells divide into liver cells and not some other cell type.
It is characterized by non-compaction of some gene promoters during mitosis. In terms of mechanism, it is believed that:
- at some point prior to the onset of mitosis, the promoters of genes that exist in a transcription-competent state become "marked" in some way,
- this "mark" persists both during and after mitosis, and
- the marking transmits gene expression memory by preventing the mitotic compaction of DNA at this locus, or by facilitating reassembly of transcription complexes on the promoter, or both.
In some cases, bookmarking is mediated by binding of specific factors to the promoter prior to onset of mitosis, but in other cases could be mediated by patterns of histone modification or presence of histone variants that are characteristic of active genes, and which are believed to persist throughout mitosis.
In the case of specific genes, for example, the stress-inducible hsp70 gene, bookmarking may also function as a mechanism for ensuring that the gene can be transcribed early in G1 phase if a stress were to occur at that time. If this gene promoter were compacted it would take time to de-compact in G1, during which time the cell would be unable to transcribe this cytoprotective gene, leaving it vulnerable to stress-induced cell death. In this case, bookmarking appears to be important for cell survival.