Abstract
Interstrand cross‐links (ICLs) are extremely toxic DNA lesions since they prevent any processes that require strand separation including DNA replication and transcription. In higher eukaryotes, the repair of these lesions takes place mainly in S‐phase, suggesting a connection to DNA replication. Many years of predominantly genetic research has shown that ICL repair requires the action of several classes of enzymes, including translesion DNA polymerases, structure‐specific endonucleases, recombinases, and numerous Fanconi anemia (FA) proteins. Using a Xenopus egg extract‐based ICL repair assay, we showed that lesion bypass during ICL repair occurs in several discrete steps that are coupled to DNA replication. We will present our latest results on how the FA proteins, BRCA1, and the recombination machinery promote replication‐coupled ICL repair.
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