Journal
MOLECULAR CELL
Volume 42, Issue 3, Pages 285-296Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2011.02.036
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Funding
- Biotechnology and Biological Sciences Research Council (BBSRC)
- Commonwealth Association
- Association for International Cancer Research, St. Andrews
- Medical Research Council
- European Union
- Cancer Research UK [C24125/A8307]
- Wellcome Trust
- Newton Trust
- Biotechnology and Biological Sciences Research Council [BB/F020236/1] Funding Source: researchfish
- Medical Research Council [G0701175] Funding Source: researchfish
- BBSRC [BB/F020236/1] Funding Source: UKRI
- MRC [G0701175] Funding Source: UKRI
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Epigenetic marks such as posttranslational histone modifications specify the functional states of underlying DNA sequences, though how they are maintained after their disruption during DNA replication remains a critical question. We identify the mammalian SWI/SNF-like protein SMARCAD1 as a key factor required for the re-establishment of repressive chromatin. The ATPase activity of SMARCAD1 is necessary for global deacetylation of histones H3/H4. In this way, SMARCAD1 promotes methylation of H3K9, the establishment of heterochromatin, and faithful chromosome segregation. SMARCAD1 associates with transcriptional repressors including KAP1, histone deacetylases HDAC1/2 and the histone methyltransferase G9a/GLP and modulates the interaction of HDAC1 and KAP1 with heterochromatin. SMARCAD1 directly interacts with PCNA, a central component of the replication machinery, and is recruited to sites of DNA replication. Our findings suggest that chromatin remodeling by SMARCAD1 ensures that silenced loci, such as pericentric heterochromatin, are correctly perpetuated.
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