A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells

• Pierangela Sabbattini ^[1] ; Claudia Canzonetta ^[1] ; Marcela Sjoberg ^[1] ; Svetlana Nikic ^[1] ; Andrew Georgiou ^[1] ; Geoffrey Kemball-Cook ^[2] ; Holger W Auner ^[1] ; Niall Dillon ^[1]
  1. [1] Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College, London, UK
  2. [2] Haemostasis and Thrombosis Group, MRC Clinical Sciences Centre, Faculty of Medicine, Imperial College, London, UK
• Localización: EMBO journal: European Molecular Biology Organization, ISSN 0261-4189, Vol. 26, Nº. 22, 2007, págs. 4657-4669
• Idioma: inglés
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• Resumen

  • Combinatorial modifications of the core histones have the potential to fine-tune the epigenetic regulation of chromatin states. The Aurora B kinase is responsible for generating the double histone H3 modification tri-methylated K9/phosphorylated S10 (H3K9me3/S10ph), which has been implicated in chromosome condensation during mitosis. In this study, we have identified a novel role for Aurora B in epigenetic marking of silent chromatin during cell differentiation. We find that phosphorylation of H3 S10 by Aurora B generates high levels of the double H3K9me3/S10ph modification in differentiated postmitotic cells and also results in delocalisation of HP1β away from heterochromatin in terminally differentiated plasma cells. Microarray analysis of the H3K9me3/S10ph modification shows a striking increase in the modification across repressed genes during differentiation of mesenchymal stem cells. Our results provide evidence that the Aurora B kinase has a role in marking silent chromatin independently of the cell cycle and suggest that targeting of Aurora B-mediated phosphorylation of H3 S10 to repressed genes could be a mechanism for epigenetic silencing of gene expression.