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A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells
Author(s) -
Sabbattini Pierangela,
Canzonetta Claudia,
Sjoberg Marcela,
Nikic Svetlana,
Georgiou Andrew,
KemballCook Geoffrey,
Auner Holger W,
Dillon Niall
Publication year - 2007
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7601875
Subject(s) - biology , chromatin , epigenetics , microbiology and biotechnology , genetics , cellular differentiation , dna , gene
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.