FANCM of the Fanconi anemia core complex is required for both monoubiquitination and DNA repair

摘要: In response to DNA damage, the Fanconi anemia (FA) core complex functions as a signaling machine for monoubiquitination of FANCD2 and FANCI. It remains unclear whether this can also participate in subsequent repair. We have shown previously that FANCM constituent contains highly conserved helicase domain an associated ATP-dependent translocase activity. Here we show possesses ATP-independent binding activity bi-directional branch-point translocation on synthetic four-way junction DNA, which mimics intermediates generated during homologous recombination or at stalled replication forks. Using siRNA-based complementation system, found activities are required cellular resistance DNA-crosslinking drug, mitomycin C, but not contrast, requires entire FANCM, has both ATP dependent independent activities. These data consistent with participation its FA pathway through ensuing