A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells
Abstract 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 implicate...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Sabbattini, Pierangela [verfasserIn] Canzonetta, Claudia [verfasserIn] Sjoberg, Marcela [verfasserIn] Nikic, Svetlana [verfasserIn] Georgiou, Andrew [verfasserIn] Kemball‐Cook, Geoffrey [verfasserIn] Auner, Holger W [verfasserIn] Dillon, Niall [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2007 |
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| Schlagwörter: |
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| Anmerkung: |
© European Molecular Biology Organization 2007 |
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| Übergeordnetes Werk: |
Enthalten in: The EMBO Journal - Nature Publishing Group UK, 2023, 26(2007), 22 vom: 18. Okt., Seite 4657-4669 |
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| Übergeordnetes Werk: |
volume:26 ; year:2007 ; number:22 ; day:18 ; month:10 ; pages:4657-4669 |
| Links: |
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| DOI / URN: |
10.1038/sj.emboj.7601875 |
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| Katalog-ID: |
SPR057857784 |
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| 100 | 1 | |a Sabbattini, Pierangela |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells |
| 264 | 1 | |c 2007 | |
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| 520 | |a Abstract 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. | ||
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| 650 | 4 | |a epigenetic regulation |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Canzonetta, Claudia |e verfasserin |4 aut | |
| 700 | 1 | |a Sjoberg, Marcela |e verfasserin |4 aut | |
| 700 | 1 | |a Nikic, Svetlana |e verfasserin |4 aut | |
| 700 | 1 | |a Georgiou, Andrew |e verfasserin |4 aut | |
| 700 | 1 | |a Kemball‐Cook, Geoffrey |e verfasserin |4 aut | |
| 700 | 1 | |a Auner, Holger W |e verfasserin |4 aut | |
| 700 | 1 | |a Dillon, Niall |e verfasserin |4 aut | |
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10.1038/sj.emboj.7601875 doi (DE-627)SPR057857784 (SPR)sj.emboj.7601875-e DE-627 ger DE-627 rakwb eng Sabbattini, Pierangela verfasserin aut A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2007 Abstract 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. Aurora B (dpeaa)DE-He213 chromatin (dpeaa)DE-He213 epigenetic regulation (dpeaa)DE-He213 Canzonetta, Claudia verfasserin aut Sjoberg, Marcela verfasserin aut Nikic, Svetlana verfasserin aut Georgiou, Andrew verfasserin aut Kemball‐Cook, Geoffrey verfasserin aut Auner, Holger W verfasserin aut Dillon, Niall verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 26(2007), 22 vom: 18. Okt., Seite 4657-4669 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:26 year:2007 number:22 day:18 month:10 pages:4657-4669 https://dx.doi.org/10.1038/sj.emboj.7601875 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 26 2007 22 18 10 4657-4669 |
| spelling |
10.1038/sj.emboj.7601875 doi (DE-627)SPR057857784 (SPR)sj.emboj.7601875-e DE-627 ger DE-627 rakwb eng Sabbattini, Pierangela verfasserin aut A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2007 Abstract 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. Aurora B (dpeaa)DE-He213 chromatin (dpeaa)DE-He213 epigenetic regulation (dpeaa)DE-He213 Canzonetta, Claudia verfasserin aut Sjoberg, Marcela verfasserin aut Nikic, Svetlana verfasserin aut Georgiou, Andrew verfasserin aut Kemball‐Cook, Geoffrey verfasserin aut Auner, Holger W verfasserin aut Dillon, Niall verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 26(2007), 22 vom: 18. Okt., Seite 4657-4669 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:26 year:2007 number:22 day:18 month:10 pages:4657-4669 https://dx.doi.org/10.1038/sj.emboj.7601875 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 26 2007 22 18 10 4657-4669 |
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10.1038/sj.emboj.7601875 doi (DE-627)SPR057857784 (SPR)sj.emboj.7601875-e DE-627 ger DE-627 rakwb eng Sabbattini, Pierangela verfasserin aut A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2007 Abstract 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. Aurora B (dpeaa)DE-He213 chromatin (dpeaa)DE-He213 epigenetic regulation (dpeaa)DE-He213 Canzonetta, Claudia verfasserin aut Sjoberg, Marcela verfasserin aut Nikic, Svetlana verfasserin aut Georgiou, Andrew verfasserin aut Kemball‐Cook, Geoffrey verfasserin aut Auner, Holger W verfasserin aut Dillon, Niall verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 26(2007), 22 vom: 18. Okt., Seite 4657-4669 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:26 year:2007 number:22 day:18 month:10 pages:4657-4669 https://dx.doi.org/10.1038/sj.emboj.7601875 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 26 2007 22 18 10 4657-4669 |
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10.1038/sj.emboj.7601875 doi (DE-627)SPR057857784 (SPR)sj.emboj.7601875-e DE-627 ger DE-627 rakwb eng Sabbattini, Pierangela verfasserin aut A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2007 Abstract 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. Aurora B (dpeaa)DE-He213 chromatin (dpeaa)DE-He213 epigenetic regulation (dpeaa)DE-He213 Canzonetta, Claudia verfasserin aut Sjoberg, Marcela verfasserin aut Nikic, Svetlana verfasserin aut Georgiou, Andrew verfasserin aut Kemball‐Cook, Geoffrey verfasserin aut Auner, Holger W verfasserin aut Dillon, Niall verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 26(2007), 22 vom: 18. Okt., Seite 4657-4669 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:26 year:2007 number:22 day:18 month:10 pages:4657-4669 https://dx.doi.org/10.1038/sj.emboj.7601875 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 26 2007 22 18 10 4657-4669 |
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10.1038/sj.emboj.7601875 doi (DE-627)SPR057857784 (SPR)sj.emboj.7601875-e DE-627 ger DE-627 rakwb eng Sabbattini, Pierangela verfasserin aut A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells 2007 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © European Molecular Biology Organization 2007 Abstract 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. Aurora B (dpeaa)DE-He213 chromatin (dpeaa)DE-He213 epigenetic regulation (dpeaa)DE-He213 Canzonetta, Claudia verfasserin aut Sjoberg, Marcela verfasserin aut Nikic, Svetlana verfasserin aut Georgiou, Andrew verfasserin aut Kemball‐Cook, Geoffrey verfasserin aut Auner, Holger W verfasserin aut Dillon, Niall verfasserin aut Enthalten in The EMBO Journal Nature Publishing Group UK, 2023 26(2007), 22 vom: 18. Okt., Seite 4657-4669 (DE-627)266022529 (DE-600)1467419-1 1460-2075 nnns volume:26 year:2007 number:22 day:18 month:10 pages:4657-4669 https://dx.doi.org/10.1038/sj.emboj.7601875 X:SPRINGER Resolving-System kostenfrei Volltext SYSFLAG_0 GBV_SPRINGER GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_72 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_168 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_252 GBV_ILN_266 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2018 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4029 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4155 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 26 2007 22 18 10 4657-4669 |
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Sabbattini, Pierangela @@aut@@ Canzonetta, Claudia @@aut@@ Sjoberg, Marcela @@aut@@ Nikic, Svetlana @@aut@@ Georgiou, Andrew @@aut@@ Kemball‐Cook, Geoffrey @@aut@@ Auner, Holger W @@aut@@ Dillon, Niall @@aut@@ |
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Sabbattini, Pierangela |
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Sabbattini, Pierangela misc Aurora B misc chromatin misc epigenetic regulation A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells |
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A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells Aurora B (dpeaa)DE-He213 chromatin (dpeaa)DE-He213 epigenetic regulation (dpeaa)DE-He213 |
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A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells |
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Sabbattini, Pierangela Canzonetta, Claudia Sjoberg, Marcela Nikic, Svetlana Georgiou, Andrew Kemball‐Cook, Geoffrey Auner, Holger W Dillon, Niall |
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a novel role for the aurora b kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells |
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A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells |
| abstract |
Abstract 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. © European Molecular Biology Organization 2007 |
| abstractGer |
Abstract 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. © European Molecular Biology Organization 2007 |
| abstract_unstemmed |
Abstract 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. © European Molecular Biology Organization 2007 |
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A novel role for the Aurora B kinase in epigenetic marking of silent chromatin in differentiated postmitotic cells |
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Canzonetta, Claudia Sjoberg, Marcela Nikic, Svetlana Georgiou, Andrew Kemball‐Cook, Geoffrey Auner, Holger W Dillon, Niall |
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| score |
7.4003687 |