Fanconi anemia (FA) is a recessive genetic disorder characterized by hypersensitivity to
crosslinking agents that has been attributed to defects in DNA repair and/or replication.
FANCD2 and the FA core complex bind to chromatin during DNA replication; however, the
role of FA proteins during replication is unknown. Using Xenopus cell-free extracts, we show
that FANCL depletion results in defective DNA replication restart following treatment with
camptothecin, a drug that results in DSBs during DNA replication. This defect is more …