Bookmarking 1431111 210995592 2008-05-08T09:33:00Z Bongwarrior 1879566 changed {{otheruses}}, the disambiguation page is going to be moved shortly {{otheruses|Bookmark (disambiguation)}} 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 (biology)|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 promoter]]s 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 (genetics)|transcription]]-competent state become "marked" in some way, * that this "mark" persists both during and after [[mitosis]], * and that 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. ==References== * Sarge, K.D. and Park-Sarge, O.K. (2005) Gene bookmarking: keeping the pages open. Trends Biochem. Sci. 30, 605–610. * John, S. and Workman, J.L. (1998) Bookmarking genes for activation in condensed mitotic chromosomes. Bioessays 20, 275–279. * Xing et al. (2005) Mechanism of hsp70i gene bookmarking. Science 307, 421–423. * Michelotti, E.F. et al. (1997) Marking of active genes on mitotic chromosomes. Nature 388, 895–899. * Christova, R. and Oelgeschlager, T. (2002) Association of human TFIID-promoter complexes with silenced mitotic chromatin in vivo. Nat. Cell. Biol. 4, 79–82. * Kouskouti, A. and Talianidis, I. (2005) Histone modifications defining active genes persist after transcriptional and mitotic inactivation. EMBO J. 24, 347–357. * Chow, C.M. et al. (2005) Variant histone H3.3 marks promoters of transcriptionally active genes during mammalian cell division. EMBO Rep. 6, 354–360. [[Category:Genetics]] [[Category:Epigenetics]] {{genetics-stub}}