The Fanconi Anemia Pathway Promotes Replication-Dependent DNA Interstrand Cross-Link Repair
作者： P. Knipscheer , M. Raschle , A. Smogorzewska , M. Enoiu , T. V. Ho
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摘要: Fanconi anemia is a human cancer predisposition syndrome caused by mutations in 13 Fanc genes. The disorder characterized genomic instability and cellular hypersensitivity to chemicals that generate DNA interstrand cross-links (ICLs). A central event the activation of pathway mono-ubiquitylation FANCI-FANCD2 complex, but how this complex confers ICL resistance remains enigmatic. Using cell-free system, we showed required for replication-coupled repair S phase. Removal FANCD2 from extracts inhibits both nucleolytic incisions near translesion synthesis past lesion. Reversal these defects requires ubiquitylated FANCI-FANCD2. Our results show multiple steps essential S-phase mechanism fail when compromised.
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