Figure 3.

Current model for replication-independent ICL repair. If an ICL occurs in nonreplicating cells, it may be recognized by interfering with transcription or because it induces helix distortion, which is recognized by the nucleotide excision repair pathway. This could trigger recruitment of downstream NER factors including XPF-ERCC1. Incisions around the lesion on one strand of DNA unhook the lesion from that strand. Translesion polymerases can bypass the ICL and fill the gap with new DNA synthesis. This is sufficient to restore double-strand DNA that is free of interstrand cross-links.