Cited by 39Genomics and Chromatin DynamicsChromatin Remodeling and CancerEpigenetics and DNA Methylation

Chromatin Remodelling by WSTF-ISWI at the Replication Site: Opening a Window of Opportunity for Epigenetic Inheritance?

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Poot, Raymond A., Bozhenok, Ludmila, Berg, Debbie L.C. van den, Hawkes, Nicola, Varga-Weisz, Patrick D.·2005·Cell Cycle

Abstract

During DNA replication, chromatin states have to be accurately transmitted from the parental to the daughter strands for faithful epigenetic inheritance. Chromatin remodelling factors at the replication site are thought to be involved in this process. Recent work adds ATP-dependent nucleosome remodelling factors to this category of enzymes. The WICH complex, consisting of the ISWI-type ATPase SNF2H and the Williams Syndrome Transcription Factor (WSTF), binds to replication foci using PCNA, a key factor in DNA- and chromatin replication and DNA repair, as an interaction platform. Depletion of WSTF results in decreased chromatin accessibility, which is evident already in newly replicated DNA. This leads to heterochromatin formation on a global scale and a decrease in overall transcriptional activity. Here, we propose that WICH, by keeping nucleosomes mobile, provides access to the newly replicated DNA and may thereby create a window of opportunity after DNA replication for rebinding of factors that maintain the epigenetic state, and thus prevents aberrant heterochromatin formation. Our model may provide an explanation for the long-standing observation of a delay in chromatin "maturation" on newly replicated DNA, by connecting this delay with the action of PCNA-bound WSTF-ISWI, and highlights chromatin remodeling shortly after DNA replication as a critical point for regulation.

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Research works printed but not linked: 33

  1. McNairn AJ, Gilbert DM. Epigenomic replication: linking epigenetics to DNA replication. Bioessays 2003; 25:647-56.
  2. Schreiber SL, Bernstein BE. Signaling network model of chromatin. Cell 2002; 111:771-8.
  3. Grewal SI, Elgin SC. Heterochromatin: new possibilities for the inheritance of structure. Curr Opin Genet Dev 2002; 12: 178-87.
  4. Lucchini R, Wellinger RE, Sogo JM. Nucleosome positioning at the replication fork. EMBO J 2001; 20: 7294-302.
  5. Gasser R, Koller T, Sogo JM. The stability of nucleosomes at the replication fork. J Mol Biol 1996; 258: 224-39.
  6. Lucchini R ,Sogo J M. Replication of transcriptionally active chromatin. Nature 1995; 374: 276-80.
  7. Fletcher TM, Hansen JC. The nucleosomal array: structure/function relationships. Crit Rev Eukaryot Gene Expr 1996; 6: 149-88.
  8. Becker PB. Nucleosome sliding: facts and fiction. EMBO J 2002; 21:4749-53.
  9. Becker PB, Horz W. ATP-dependent nucleosome remodeling. Annu Rev Biochem 2002; 71:247-73.
  10. Lusser A, Kadonaga JT. Chromatin remodeling by ATP-dependent molecular machines. Bioessays 2003; 25:1192-200.
  11. Corona DF, Tamkun JW. Multiple roles for ISWI in transcription, chromosome organiza- tion and DNA replication. Biochim Biophys Acta 2004; 1677:113-9.
  12. Cho KS, Elizondo LI, Boerkoel CF. Advances in chromatin remodeling and human disease. Curr Opin Genet Dev 2004; 14:308-15.
  13. Bozhenok L, Wade PA ,Varga-Weisz P. WSTF-ISWI chromatin remodeling complex targets heterochromatic replication foci. EMBO J 2002; 21:2231-41.
  14. Francke U. Williams-Beuren syndrome: genes and mechanisms. Hum Mol Genet 1999; 8:1947-54.
  15. Poot RA, Bozhenok L, van den Berg DL, Steffensen S, Ferreira F, Grimaldi M, Gilbert N, Ferreira J, Varga-Weisz PD. The Williams syndrome transcription factor interacts with PCNA to target chromatin remodelling by ISWI to replication foci. Nat Cell Biol 2004; 6:1236-44.
  16. Pombo A, Jackson DA, Hollinshead M, Wang Z, Roeder RG, Cook PR. Regional special- ization in human nuclei: visualization of discrete sites of transcription by RNA polymerase III. EMBO J 1999; 18:2241-53. Cell Cycle 2005; Vol. 4 Issue 4
  17. Jackson DA, Iborra FJ, Manders EM, Cook PR. Numbers and organization of RNA poly- merases, nascent transcripts, and transcription units in HeLa nuclei. Mol Biol Cell 1998; 9:1523-36.
  18. Shibahara K, Stillman B. Replication-dependent marking of DNA by PCNA facilitates CAF-1-coupled inheritance of chromatin. Cell 1999; 96:575-85.
  19. Sporbert A, Gahl A, Ankerhold R, Leonhardt H, Cardoso MC. DNA polymerase clamp shows little turnover at established replication sites but sequential de novo assembly at adja- cent origin clusters. Mol Cell 2002; 10:1355-65.
  20. Maga G, Hubscher U. Proliferating cell nuclear antigen (PCNA): a dancer with many part- ners. J Cell Sci 2003; 116:3051-60.
  21. Jonsson ZO, Hubscher U. Proliferating cell nuclear antigen: more than a clamp for DNA polymerases. Bioessays 1997; 19:967-75.
  22. Hoege C, Pfander B, Moldovan GL, Pyrowolakis G, Jentsch S. RAD6-dependent DNA repair is linked to modification of PCNA by ubiquitin and SUMO. Nature 2002; 419:135-41.
  23. O'Donnell M. Processivity factors. Curr Biol 1999; 9: R545.
  24. Li X, Li J, Harrington J, Lieber MR, Burgers PM. Lagging strand DNA synthesis at the eukaryotic replication fork involves binding and stimulation of FEN-1 by proliferating cell nuclear antigen. J Biol Chem 1995; 270:22109-12.
  25. Iida T, Suetake I, Tajima S, Morioka H, Ohta S, Obuse C, Tsurimoto T. PCNA clamp facil- itates action of DNA cytosine methyltransferase 1 on hemimethylated DNA. Genes Cells 2002; 7:997-1007.
  26. Leonhardt H, Page AW, Weier HU, Bestor TH. A targeting sequence directs DNA methyl- transferase to sites of DNA replication in mammalian nuclei. Cell 1992; 71:865-73.
  27. Hong R, Chakravarti D. The human proliferating cell nuclear antigen regulates transcrip- tional coactivator p300 activity and promotes transcriptional repression. J Biol Chem 2003; 278:44505-13.
  28. Schlaeger EJ, Pulm W, Knippers R. Chromatin maturation depends on continued DNA- replication. FEBS Lett 1983; 156:281-6.
  29. Klempnauer KH, Fanning E, Otto B, Knippers R. Maturation of newly replicated chro- matin of simian virus 40 and its host cell. J Mol Biol 1980; 136:359-74.
  30. Cusick ME, Lee KS, DePamphilis ML, Wassarman PM. Structure of chromatin at deoxyri- bonucleic acid replication forks: nuclease hypersensitivity results from both prenucleosomal deoxyribonucleic acid and an immature chromatin structure. Biochemistry 1983; 22:3873-84.
  31. Kitagawa H, Fujiki R, Yoshimura K, Mezaki Y, Uematsu Y, Matsui D, Ogawa S, Unno K, Okubo M, Tokita A, Nakagawa T, Ito T, Ishimi Y, Nagasawa H, Matsumoto T, Yanagisawa J, Kato S. The chromatin-remodeling complex WINAC targets a nuclear receptor to pro- moters and is impaired in Williams syndrome. Cell 2003; 113:905-17.
  32. Murzina N, Verreault A, Laue E, Stillman B. Heterochromatin dynamics in mouse cells: interaction between chromatin assembly factor 1 and HP1 proteins. Mol Cell 1999; 4:529-40.
  33. Quivy JP, Roche D, Kirschner D, Tagami H, Nakatani Y, Almouzni G. A CAF-1 depen- dent pool of HP1 during heterochromatin duplication. EMBO J 2004; 23:3516-26.

Cited by

Sorted by citations

Authors
Poot, R. A., Bozhenok, L., Berg, D. L. C. V. D., Hawkes, N., & Varga-Weisz, P. D.
Affiliations
  • Imperial College London (GB)
  • Babraham Institute (GB)
  • Erasmus MC (NL)
Venue
Cell Cycle
Published
2005-01-28
Volume
4
Issue
4
Pages
543-546
ISSN
  • 1538-4101 (ISSN-L)
  • 1551-4005
OpenAlex
W2312946532
Cited by
39
References
0
Citations by year
2025: 1 · 2021: 1 · 2020: 2 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 3 · 2015: 1 · 2014: 3 · 2013: 3 · 2012: 5
FWCI
0.38
Type
journal article
Language
en
Open access
Locations
  • Cell Cycle (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Marie Curie
  • Directorate for Biological Sciences
  • Biotechnology and Biological Sciences Research Council
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
Keywords
chromatin remodeling, WSTF, ISWI, DNA replication, epigenetic inheritance, PCNA, nucleosome remodeling, heterochromatin formation, chromatin accessibility, SNF2H, replication foci
MeSH terms
Bromodomain Containing Proteins, Adenosine Triphosphatases, Animals, Binding Sites, Cell Cycle, Chromatin, DNA, DNA Replication, Gene Expression Regulation, Heterochromatin, Humans, Models, Biological, Nucleosomes, Protein Binding, Transcription Factors, Epigenesis, Genetic

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