Journal
EMBO JOURNAL
Volume 31, Issue 17, Pages 3524-3536Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/emboj.2012.197
Keywords
DNA repair; FANCD2; FANCI; Fanconi anaemia; histone chaperone
Categories
Funding
- 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
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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
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