Bookmarking (also "gene bookmarking" or "mitotic bookmarking") refers to a potential mechanism of transmission of gene expression programs through cell division.

During mitosis, gene transcription is silenced and most transcription factors are removed from chromatin.[1][2] The term bookmarking compares transcription to reading from a book. The pause in transcription during mitosis is like closing the book. "Molecular bookmarks" are the factors that allow transcription to resume in an orderly fashion in newborn cells following mitosis (when the book is re-opened).

Bookmarks fulfill the following criteria:

  • 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.

Bookmarking as selective maintenance of an open chromatin state

The term bookmarking was originally coined to describe the non-compaction of some gene promoters during mitosis.[3] More recently genome accessibility during interphase and mitosis has been directly compared on a genome-wide scale.[4] While gene promoters tend to be better preserved than distal regulatory elements, substantial variation exists at individual sites.

Bookmarking by DNA methylation, histone post-translation modification, and histone variants

Some patterns of histone modification and the presence of some histone variants on DNA remain unchanged during mitosis and have the potential to act as bookmarks.[5][6][7] Patterns of DNA methylation are generally unchanged and also have the potential to function as bookmarks.

Bookmarking by transcription factors

Notable transcription factors implicated in mitotic bookmarking include:

References

  1. ↑ Sarge, K. D.; Park-Sarge, O. K. (2005). "Gene bookmarking: Keeping the pages open". Trends in Biochemical Sciences. 30 (11): 605–10. doi:10.1016/j.tibs.2005.09.004. PMID 16188444.
  2. ↑ Martínez-Balbás, M. A.; Dey, A; Rabindran, S. K.; Ozato, K; Wu, C (1995). "Displacement of sequence-specific transcription factors from mitotic chromatin". Cell. 83 (1): 29–38. doi:10.1016/0092-8674(95)90231-7. PMID 7553870.
  3. ↑ John, S; Workman, J. L. (1998). "Bookmarking genes for activation in condensed mitotic chromosomes". BioEssays. 20 (4): 275–9. doi:10.1002/(SICI)1521-1878(199804)20:4<275::AID-BIES1>3.0.CO;2-P. PMID 9619097.
  4. ↑ Hsiung, C. C.; Morrissey, C. S.; Udugama, M; Frank, C. L.; Keller, C. A.; Baek, S; Giardine, B; Crawford, G. E.; Sung, M. H.; Hardison, R. C.; Blobel, G. A. (2015). "Genome accessibility is widely preserved and locally modulated during mitosis". Genome Research. 25 (2): 213–25. doi:10.1101/gr.180646.114. PMC 4315295. PMID 25373146.
  5. ↑ Wang, F; Higgins, J. M. (2013). "Histone modifications and mitosis: Countermarks, landmarks, and bookmarks". Trends in Cell Biology. 23 (4): 175–84. doi:10.1016/j.tcb.2012.11.005. PMID 23246430.
  6. ↑ Kouskouti, A; Talianidis, I (2005). "Histone modifications defining active genes persist after transcriptional and mitotic inactivation". The EMBO Journal. 24 (2): 347–57. doi:10.1038/sj.emboj.7600516. PMC 545808. PMID 15616580.
  7. ↑ Chow, C. M.; Georgiou, A; Szutorisz, H; Maia e Silva, A; Pombo, A; Barahona, I; Dargelos, E; Canzonetta, C; Dillon, N (2005). "Variant histone H3.3 marks promoters of transcriptionally active genes during mammalian cell division". EMBO Reports. 6 (4): 354–60. doi:10.1038/sj.embor.7400366. PMC 1299280. PMID 15776021.
  8. ↑ Dey, A; Ellenberg, J; Farina, A; Coleman, A. E.; Maruyama, T; Sciortino, S; Lippincott-Schwartz, J; Ozato, K (2000). "A bromodomain protein, MCAP, associates with mitotic chromosomes and affects G(2)-to-M transition". Molecular and Cellular Biology. 20 (17): 6537–49. doi:10.1128/mcb.20.17.6537-6549.2000. PMC 86127. PMID 10938129.
  9. ↑ Dey, A; Nishiyama, A; Karpova, T; McNally, J; Ozato, K (2009). "Brd4 marks select genes on mitotic chromatin and directs postmitotic transcription". Molecular Biology of the Cell. 20 (23): 4899–909. doi:10.1091/mbc.E09-05-0380. PMC 2785733. PMID 19812244.
  10. ↑ Kadauke, S; Udugama, M. I.; Pawlicki, J. M.; Achtman, J. C.; Jain, D. P.; Cheng, Y; Hardison, R. C.; Blobel, G. A. (2012). "Tissue-specific mitotic bookmarking by hematopoietic transcription factor GATA1". Cell. 150 (4): 725–37. doi:10.1016/j.cell.2012.06.038. PMC 3425057. PMID 22901805.
  11. ↑ Xing, H; Wilkerson, D. C.; Mayhew, C. N.; Lubert, E. J.; Skaggs, H. S.; Goodson, M. L.; Hong, Y; Park-Sarge, O. K.; Sarge, K. D. (2005). "Mechanism of hsp70i gene bookmarking". Science. 307 (5708): 421–3. Bibcode:2005Sci...307..421X. doi:10.1126/science.1106478. PMID 15662014.
  12. ↑ Christova, R; Oelgeschläger, T (2002). "Association of human TFIID-promoter complexes with silenced mitotic chromatin in vivo". Nature Cell Biology. 4 (1): 79–82. doi:10.1038/ncb733. PMID 11744923.
  13. ↑ Festuccia, N; Dubois, A; Vandormael-Pournin, S; Gallego Tejeda, E; Mouren, A; Bessonnard, S; Mueller, F; Proux, C; Cohen-Tannoudji, M; Navarro, P (November 2016). "Mitotic binding of Esrrb marks key regulatory regions of the pluripotency network" (PDF). Nature Cell Biology. 18 (11): 1139–1148. doi:10.1038/ncb3418. PMID 27723719.
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