Ontology type: schema:ScholarlyArticle
2004-11-14
AUTHORSRaymond A. Poot, Ludmila Bozhenok, Debbie L.C. van den Berg, Søren Steffensen, Fernando Ferreira, Margaret Grimaldi, Nick Gilbert, Joao Ferreira, Patrick D. Varga-Weisz
ABSTRACTChromatin states have to be faithfully duplicated during DNA replication to maintain cell identity. It is unclear whether or how ATP-dependent chromatin-remodelling factors are involved in this process. Here we provide evidence that the Williams syndrome transcription factor (WSTF) is targeted to replication foci through direct interaction with the DNA clamp PCNA, an important coordinator of DNA and chromatin replication. WSTF, in turn, recruits imitation switch (ISWI)-type nucleosome-remodelling factor SNF2H to replication sites. These findings reveal a novel recruitment mechanism for ATP-dependent chromatin-remodelling factors that is fundamentally different from the previously documented targeting by sequence-specific transcriptional regulators. RNA-interference-mediated depletion of WSTF or SNF2H causes a compaction of newly replicated chromatin and increases the amount of heterochromatin markers, including HP1β. This increase in the amount of HP1β protein is mediated by progression through S phase and is not the result of an increase in HP1β mRNA levels. We propose that the WSTF–ISWI complex has a role in the maintenance of chromatin structures during DNA replication. More... »
PAGES1236-1244
http://scigraph.springernature.com/pub.10.1038/ncb1196
DOIhttp://dx.doi.org/10.1038/ncb1196
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PUBMEDhttps://www.ncbi.nlm.nih.gov/pubmed/15543136
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