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Epigenetic engineering shows that a human centromere resists silencing mediated by H3K27me3/K9me3
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- Nuno M. C. Martins
- Wellcome Trust Centre for Cell Biology, University of Edinburgh, Edinburgh EH9 3JR, Scotland, United Kingdom
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- Jan H. Bergmann
- Wellcome Trust Centre for Cell Biology, University of Edinburgh, Edinburgh EH9 3JR, Scotland, United Kingdom
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- Nobuaki Shono
- Laboratory of Cell Engineering, Department of Frontier Research, Kazusa DNA Research Institute, Kisarazu 292-0818, Japan
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- Hiroshi Kimura
- Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, Yokohama 226-8501, Japan
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- Vladimir Larionov
- Laboratory of Molecular Pharmacology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892
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- Hiroshi Masumoto
- Laboratory of Cell Engineering, Department of Frontier Research, Kazusa DNA Research Institute, Kisarazu 292-0818, Japan
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- William C. Earnshaw
- Wellcome Trust Centre for Cell Biology, University of Edinburgh, Edinburgh EH9 3JR, Scotland, United Kingdom
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- Kerry S. Bloom
- editor
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Description
<jats:p>Centromeres are characterized by the centromere-specific H3 variant CENP-A, which is embedded in chromatin with a pattern characteristic of active transcription that is required for centromere identity. It is unclear how centromeres remain transcriptionally active despite being flanked by repressive pericentric heterochromatin. To further understand centrochromatin’s response to repressive signals, we nucleated a Polycomb-like chromatin state within the centromere of a human artificial chromosome (HAC) by tethering the methyltransferase EZH2. This led to deposition of the H3K27me3 mark and PRC1 repressor binding. Surprisingly, this state did not abolish HAC centromere function or transcription, and this apparent resistance was not observed on a noncentromeric locus, where transcription was silenced. Directly tethering the reader/repressor PRC1 bypassed this resistance, inactivating the centromere. We observed analogous responses when tethering the heterochromatin Editor Suv39h1-methyltransferase domain (centromere resistance) or reader HP1α (centromere inactivation), respectively. Our results reveal that the HAC centromere can resist repressive pathways driven by H3K9me3/H3K27me3 and may help to explain how centromeres are able to resist inactivation by flanking heterochromatin.</jats:p>
Journal
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- Molecular Biology of the Cell
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Molecular Biology of the Cell 27 (1), 177-196, 2016-01
American Society for Cell Biology (ASCB)
