Fanconi anemia (FA) is a disorder associated with a failure in DNA repair. FANCM (defective in FA complementation group M) and its partner FAAP24 target other FA proteins to sites of DNA damage. FANCM-FAAP24 is related to XPF/MUS81 endonucleases but lacks endonucleolytic activity. We report a structure of an FANCM C-terminal fragment (FANCMCTD) bound to FAAP24 and DNA. This S-shaped structure reveals the FANCM (HhH)2 domain is buried, whereas the FAAP24 (HhH)2 domain engages DNA. We identify a second DNA contact and a metal center within the FANCM pseudo-nuclease domain and demonstrate that mutations in either region impair double-stranded DNA binding in vitro and FANCM-FAAP24 function in vivo. We show the FANCM translocase domain lies in proximity to FANCMCTD by electron microscopy and that binding fork DNA structures stimulate its ATPase activity. This suggests a tracking model for FANCM-FAAP24 until an encounter with a stalled replication fork triggers ATPase-mediated fork remodeling.
Architecture and DNA recognition elements of the Fanconi anemia FANCM-FAAP24 complex.
范可尼贫血 FANCM-FAAP24 复合物的结构和 DNA 识别元件
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作者:Coulthard Rachel, Deans Andrew J, Swuec Paolo, Bowles Maureen, Costa Alessandro, West Stephen C, McDonald Neil Q
| 期刊: | Structure | 影响因子: | 4.300 |
| 时间: | 2013 | 起止号: | 2013 Sep 3; 21(9):1648-58 |
| doi: | 10.1016/j.str.2013.07.006 | ||
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