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A conserved DNA repair response is defective in the human genetic illness Fanconi anemia (FA). Mutation of some FA genes impairs homologous recombination and error-prone DNA repair, rendering FA cells sensitive to DNA cross-linking agents. We found a genetic interaction between the FA gene FANCC and the nonhomologous end joining (NHEJ) factor Ku70. Disruption of both FANCC and Ku70 suppresses sensitivity to cross-linking agents, diminishes chromosome breaks, and reverses defective homologous recombination. Ku70 binds directly to free DNA ends, committing them to NHEJ repair. We show that purified FANCD2, a downstream effector of the FA pathway, might antagonize Ku70 activity by modifying such DNA substrates. These results reveal a function for the FA pathway in processing DNA ends, thereby diverting double-strand break repair away from abortive NHEJ and toward homologous recombination.

Original publication




Journal article



Publication Date





219 - 223


Animals, Antigens, Nuclear, Cell Line, Chickens, Chromosome Breakage, Cross-Linking Reagents, DNA Breaks, Double-Stranded, DNA Repair, DNA-Binding Proteins, Fanconi Anemia Complementation Group C Protein, Fanconi Anemia Complementation Group D2 Protein, Gene Conversion, Genes, Immunoglobulin, Humans, Immunoglobulin M, Ku Autoantigen, Point Mutation, Recombinant Proteins, Recombination, Genetic