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Smith OK, Kim R, Fu H, et al. Distinct epigenetic features of differentiation-regulated replication origins. Epigenetics Chromatin. 2016;9:18doi: 10.1186/s13072-016-0067-3.
Smith, O. K., Kim, R., Fu, H., Martin, M. M., Lin, C. M., Utani, K., Zhang, Y., Marks, A. B., Lalande, M., Chamberlain, S., Libbrecht, M. W., Bouhassira, E. E., Ryan, M. C., Noble, W. S., & Aladjem, M. I. (2016). Distinct epigenetic features of differentiation-regulated replication origins. Epigenetics & chromatin, 918. https://doi.org/10.1186/s13072-016-0067-3
Smith, Owen K, et al. "Distinct epigenetic features of differentiation-regulated replication origins." Epigenetics & chromatin vol. 9 (2016): 18. doi: https://doi.org/10.1186/s13072-016-0067-3
Smith OK, Kim R, Fu H, Martin MM, Lin CM, Utani K, Zhang Y, Marks AB, Lalande M, Chamberlain S, Libbrecht MW, Bouhassira EE, Ryan MC, Noble WS, Aladjem MI. Distinct epigenetic features of differentiation-regulated replication origins. Epigenetics Chromatin. 2016 May 10;9:18. doi: 10.1186/s13072-016-0067-3. eCollection 2016. PMID: 27168766; PMCID: PMC4862150.
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Epigenetics Chromatin. 2016 May 10;9:18. doi: 10.1186/s13072-016-0067-3. eCollection 2016.

Distinct epigenetic features of differentiation-regulated replication origins.

Epigenetics & chromatin

Owen K Smith, RyanGuk Kim, Haiqing Fu, Melvenia M Martin, Chii Mei Lin, Koichi Utani, Ya Zhang, Anna B Marks, Marc Lalande, Stormy Chamberlain, Maxwell W Libbrecht, Eric E Bouhassira, Michael C Ryan, William S Noble, Mirit I Aladjem

Affiliations

  1. DNA Replication Group, Developmental Therapeutics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 USA.
  2. In Silico Solutions, Falls Church, VA 22033 USA.
  3. Department of Genetics and Developmental Biology, University of Connecticut Health Center, Farmington, CT 06032 USA.
  4. Department of Computer Science and Engineering, University of Washington, Seattle, WA 98195 USA.
  5. Department of Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461 USA.
  6. Department of Computer Science and Engineering, University of Washington, Seattle, WA 98195 USA ; Department of Genome Sciences, University of Washington, Seattle, WA 98195 USA.

PMID: 27168766 PMCID: PMC4862150 DOI: 10.1186/s13072-016-0067-3

Abstract

BACKGROUND: Eukaryotic genome duplication starts at discrete sequences (replication origins) that coordinate cell cycle progression, ensure genomic stability and modulate gene expression. Origins share some sequence features, but their activity also responds to changes in transcription and cellular differentiation status.

RESULTS: To identify chromatin states and histone modifications that locally mark replication origins, we profiled origin distributions in eight human cell lines representing embryonic and differentiated cell types. Consistent with a role of chromatin structure in determining origin activity, we found that cancer and non-cancer cells of similar lineages exhibited highly similar replication origin distributions. Surprisingly, our study revealed that DNase hypersensitivity, which often correlates with early replication at large-scale chromatin domains, did not emerge as a strong local determinant of origin activity. Instead, we found that two distinct sets of chromatin modifications exhibited strong local associations with two discrete groups of replication origins. The first origin group consisted of about 40,000 regions that actively initiated replication in all cell types and preferentially colocalized with unmethylated CpGs and with the euchromatin markers, H3K4me3 and H3K9Ac. The second group included origins that were consistently active in cells of a single type or lineage and preferentially colocalized with the heterochromatin marker, H3K9me3. Shared origins replicated throughout the S-phase of the cell cycle, whereas cell-type-specific origins preferentially replicated during late S-phase.

CONCLUSIONS: These observations are in line with the hypothesis that differentiation-associated changes in chromatin and gene expression affect the activation of specific replication origins.

Keywords: Cell cycle; Cellular differentiation; Chromatin; CpG islands; H3K4me3; H3K9Ac; H3K9me3; Histone modification; Origin of replication; Proliferation

References

  1. Genome Med. 2011 Jun 07;3(6):36 - PubMed
  2. EMBO J. 2004 Feb 25;23(4):897-907 - PubMed
  3. Bioessays. 2003 Dec;25(12):1158-67 - PubMed
  4. Proc Natl Acad Sci U S A. 2006 Jul 5;103(27):10236-41 - PubMed
  5. Annu Rev Biochem. 2010;79:89-130 - PubMed
  6. Cell Cycle. 2012 Feb 15;11(4):658-67 - PubMed
  7. Hum Mol Genet. 2006 Sep 1;15(17):2613-22 - PubMed
  8. Chromosome Res. 2003;11(5):403-12 - PubMed
  9. J Phys Condens Matter. 2015 Feb 18;27(6):064102 - PubMed
  10. Science. 1997 Jan 17;275(5298):343-9 - PubMed
  11. Genome Res. 2013 Nov;23(11):1774-88 - PubMed
  12. Genome Res. 2015 Dec;25(12):1873-85 - PubMed
  13. Nat Biotechnol. 2006 May;24(5):572-6 - PubMed
  14. Nat Struct Mol Biol. 2012 Aug;19(8):837-44 - PubMed
  15. Science. 1995 Nov 3;270(5237):815-9 - PubMed
  16. Mol Cell. 1998 Dec;2(6):797-806 - PubMed
  17. PLoS Genet. 2013 Jun;9(6):e1003542 - PubMed
  18. Genome Res. 2009 Dec;19(12):2288-99 - PubMed
  19. Proc Natl Acad Sci U S A. 2010 Oct 12;107(41):17668-73 - PubMed
  20. Chromosome Res. 2010 Jan;18(1):137-45 - PubMed
  21. PLoS Biol. 2008 Oct 7;6(10):e245 - PubMed
  22. Mol Syst Biol. 2014 Mar 28;10:722 - PubMed
  23. Elife. 2015 Apr 29;4:null - PubMed
  24. Nat Commun. 2015 Apr 16;6:6746 - PubMed
  25. Genome Res. 2015 Apr;25(4):544-57 - PubMed
  26. Comput Biol Chem. 2014 Dec;53 Pt A:153-65 - PubMed
  27. Nat Rev Genet. 2007 Aug;8(8):588-600 - PubMed
  28. J Mol Biol. 2014 Oct 9;426(20):3330-41 - PubMed
  29. Nat Commun. 2015 May 19;6:7051 - PubMed
  30. Proc Natl Acad Sci U S A. 2008 Oct 14;105(41):15837-42 - PubMed
  31. Science. 1998 Aug 14;281(5379):1005-9 - PubMed
  32. PLoS One. 2012;7(12):e52990 - PubMed
  33. PLoS Genet. 2009 Apr;5(4):e1000446 - PubMed
  34. Exp Cell Res. 2007 Jan 1;313(1):109-20 - PubMed
  35. Subcell Biochem. 2010;50:79-104 - PubMed
  36. Mol Cell Biol. 1999 Aug;19(8):5685-95 - PubMed
  37. Curr Protoc Cell Biol. 2014 Dec 01;65:22.20.1-17 - PubMed
  38. Mol Cell Biol. 2011 Aug;31(16):3472-84 - PubMed
  39. BMC Genomics. 2015 Feb 28;16:142 - PubMed
  40. Trends Cell Biol. 2007 Jun;17(6):271-8 - PubMed
  41. Genome Res. 2011 Nov;21(11):1822-32 - PubMed
  42. J Cell Sci. 2002 Mar 1;115(Pt 5):869-72 - PubMed
  43. Chromosoma. 2014 Jun;123(3):183-99 - PubMed
  44. Nat Rev Mol Cell Biol. 2015 Jun;16(6):360-74 - PubMed
  45. Bioinformatics. 2009 Aug 1;25(15):1952-8 - PubMed
  46. Mol Biol Cell. 2010 Feb 1;21(3):393-404 - PubMed
  47. EMBO J. 1998 Apr 15;17(8):2426-35 - PubMed
  48. Curr Opin Cell Biol. 2006 Jun;18(3):231-9 - PubMed
  49. ILAR J. 2012;53(3-4):232-9 - PubMed
  50. Curr Biol. 2012 Feb 7;22(3):R81-2 - PubMed
  51. Genome Res. 2015 Aug;25(8):1091-103 - PubMed
  52. Genes Dev. 2013 Jun 15;27(12):1318-38 - PubMed
  53. J Mol Biol. 2013 Nov 29;425(23):4845-55 - PubMed
  54. Genes Dev. 2003 Aug 1;17(15):1894-908 - PubMed
  55. PLoS Genet. 2014 May 01;10(5):e1004319 - PubMed
  56. Nature. 2013 Jul 4;499(7456):88-91 - PubMed
  57. Epigenetics. 2011 Jun;6(6):665-70 - PubMed
  58. J Cell Biol. 2015 Jan 19;208(2):147-60 - PubMed
  59. Genome Res. 2015 May;25(5):725-35 - PubMed
  60. Genome Res. 2010 Jun;20(6):761-70 - PubMed
  61. PLoS Genet. 2014 May 01;10(5):e1004282 - PubMed
  62. Dev Cell. 2012 Oct 16;23(4):796-811 - PubMed
  63. Hum Mol Genet. 2014 Jun 1;23(11):2940-52 - PubMed
  64. Mol Cell Biol. 2004 Apr;24(7):2958-67 - PubMed
  65. Epigenetics. 2014 Feb;9(2):257-67 - PubMed
  66. Proc Natl Acad Sci U S A. 2010 Jan 5;107(1):139-44 - PubMed
  67. J Immunol. 2006 May 1;176(9):5446-54 - PubMed

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