Variant histone H3.3 marks promoters of transcriptionally active genes during mammalian cell division
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- Cheok‐Man Chow
- Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College, Hammersmith Campus Du Cane Road London W12 0NN UK
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- Andrew Georgiou
- Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College, Hammersmith Campus Du Cane Road London W12 0NN UK
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- Henrietta Szutorisz
- Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College, Hammersmith Campus Du Cane Road London W12 0NN UK
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- Alexandra Maia e Silva
- Instituo Superior de Ciencias da Saude‐Sul Monte da Caparica 2829‐511 Caparica Portugal
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- Ana Pombo
- Nuclear Organisation Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College, Hammersmith Campus Du Cane Road London W12 0NN UK
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- Isabel Barahona
- Instituo Superior de Ciencias da Saude‐Sul Monte da Caparica 2829‐511 Caparica Portugal
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- Elise Dargelos
- Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College, Hammersmith Campus Du Cane Road London W12 0NN UK
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- Claudia Canzonetta
- Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College, Hammersmith Campus Du Cane Road London W12 0NN UK
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- Niall Dillon
- Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College, Hammersmith Campus Du Cane Road London W12 0NN UK
説明
<jats:p>Variant histone H3.3 is incorporated into nucleosomes by a mechanism that does not require DNA replication and has also been implicated as a potential mediator of epigenetic memory of active transcriptional states. In this study, we have used chromatin immunoprecipitation analysis to show that H3.3 is found mainly at the promoters of transcriptionally active genes. We also show that H3.3 combines with H3 acetylation and K4 methylation to form a stable mark that persists during mitosis. Our results suggest that H3.3 is deposited principally through the action of chromatin‐remodelling complexes associated with transcriptional initiation, with deposition mediated by RNA polymerase II elongation having only a minor role.</jats:p>
収録刊行物
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- EMBO reports
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EMBO reports 6 (4), 354-360, 2005-04
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