期刊
EMBO JOURNAL
卷 31, 期 17, 页码 3524-3536出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/emboj.2012.197
关键词
DNA repair; FANCD2; FANCI; Fanconi anaemia; histone chaperone
资金
- Japanese Society for the Promotion of Science (JSPS)
- Ministry of Education, Culture, Sports, Science and Technology (MEXT), Japan
- Waseda Research Institute for Science and Engineering
- Sagawa Foundation for Promotion of Cancer Research
- NOVARTIS Foundation (Japan) for the Promotion of Science
- Ichiro Kanehara Foundation
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Grants-in-Aid for Scientific Research [10J02700, 20114001, 24870027, 23651046, 23590380, 23131505, 24570138, 22370063, 20114006] Funding Source: KAKEN
Fanconi anaemia (FA) is a rare hereditary disorder characterized by genomic instability and cancer susceptibility. A key FA protein, FANCD2, is targeted to chromatin with its partner, FANCI, and plays a critical role in DNA crosslink repair. However, the molecular function of chromatin-bound FANCD2-FANCI is still poorly understood. In the present study, we found that FANCD2 possesses nucleosome-assembly activity in vitro. The mobility of histone H3 was reduced in FANCD2-knockdown cells following treatment with an interstrand DNA crosslinker, mitomycin C. Furthermore, cells harbouring FANCD2 mutations that were defective in nucleosome assembly displayed impaired survival upon cisplatin treatment. Although FANCI by itself lacked nucleosome-assembly activity, it significantly stimulated FANCD2-mediated nucleosome assembly. These observations suggest that FANCD2-FANCI may regulate chromatin dynamics during DNA repair. The EMBO Journal (2012) 31, 3524-3536. doi: 10.1038/emboj.2012.197; Published online 24 July 2012 Subject Categories: genome stability & dynamics; chromatin & transcription
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据