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SETDB1, HP1 and SUV39 promote repositioning of 53BP1 to extend resection during homologous recombination in G2 cells
http://hdl.handle.net/10069/35892
http://hdl.handle.net/10069/35892c406a1ab-aa25-41c6-853c-76d67a5e40b6
名前 / ファイル | ライセンス | アクション |
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NAR43_7931.pdf (7.6 MB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2015-10-19 | |||||
タイトル | ||||||
タイトル | SETDB1, HP1 and SUV39 promote repositioning of 53BP1 to extend resection during homologous recombination in G2 cells | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Alagoz, Meryem
× Alagoz, Meryem× Katsuki, Yoko× Ogiwara, Hideaki× Ogi, Tomoo× Shibata, Atsushi× Kakarougkas, Andreas× Jeggo, Penny |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Recent studies have shown that homologous recombination (HR) requires chromatin repression as well as relaxation at DNA double strand breaks (DSBs). HP1 and SUV39H1/2 are repressive factors essential for HR. Here, we identify SETDB1 as an additional compacting factor promoting HR. Depletion of HP1, SUV39, SETDB1 or BRCA1 confer identical phenotypes. The repressive factors, like BRCA1, are dispensable for the initiation of resection but promote the extension step causing diminished RPA or RAD51 foci and HR in irradiated G2 cells. Depletion of the compacting factors does not inhibit BRCA1 recruitment but at 8 h post IR, BRCA1 foci are smaller and aberrantly positioned compared to control cells. BRCA1 promotes 53BP1 repositioning to the periphery of enlarged foci and formation of a devoid core with BRCA1 becoming enlarged and localized internally to 53BP1. Depletion of the compacting factors precludes these changes at irradiation-induced foci. Thus, the repressive factors are required for BRCA1 function in promoting the repositioning of 53BP1 during HR. Additionally, depletion of these repressive factors in undamaged cells causes diminished sister chromatid association at centromeric sequences. We propose a model for how these findings may be functionally linked. | |||||
書誌情報 |
Nucleic Acids Research 巻 43, 号 16, p. 7931-7944, 発行日 2015-09-18 |
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出版者 | ||||||
出版者 | Oxford University Press | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 03051048 | |||||
EISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 13624962 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1093/nar/gkv722 | |||||
権利 | ||||||
権利情報 | c The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research. | |||||
権利 | ||||||
権利情報 | This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited. | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | Nucleic Acids Research, 43(16), pp.7931-7911; 2015 |