Effects of replication domains on genome-wide UV-induced DNA damage and repair
Nucleotide excision repair is the primary repair mechanism that removes UV-induced DNA lesions in placentals. Unrepaired UV-induced lesions could result in mutations during DNA replication. Although the mutagenesis of pyrimidine dimers is reasonably well understood, the direct effects of replication fork progression on nucleotide excision repair are yet to be clarified. Here, we applied Damage-seq and XR-seq techniques and generated replication maps in synchronized UV-treated HeLa cells. The results suggest that ongoing replication stimulates local repair in both early and late replication domains. Additionally, it was revealed that lesions on lagging strand templates are repaired slower in late replication domains, which is probably due to the imbalanced sequence context. Asymmetric relative repair is in line with the strand bias of melanoma mutations, suggesting a role of exogenous damage, repair, and replication in mutational strand asymmetry.
- The Mfd protein is the Transcription-Repair Coupling Factor (TRCF) in Mycobacterium smegmatis
- Genome-wide Excision Repair Map of Cyclobutane Pyrimidine Dimers in Arabidopsis and the Roles of CSA1 and CSA2 Proteins in Transcription-Coupled Repair
- CSB-independent, XPC-dependent transcription-coupled repair in Drosophila.
- Comparative analyses of two primate species diverged by more than 60 million years show different rates but similar distribution of genome-wide UV repair events
- Nucleotide excision repair capacity increases during differentiation of human embryonic carcinoma cells into neurons and muscle cells
- Differential damage and repair of anti-cancer drug cisplatin induced DNA-adducts across mouse organs
- Genome-wide mapping of nucleotide excision repair with XR-seq.
- Cisplatin-DNA adduct repair of transcribed genes is controlled by two circadian programs in mouse tissues.
- Genome-wide Excision Repair in Arabidopsis is coupled to transcription and reflects circadian gene expression patterns.
- Single-nucleotide resolution dynamic repair maps of UV damage in Saccharomyces cerevisiae genome.
- Mfd translocase is necessary and sufficient for transcription-coupled repair in Escherichia coli.
- Molecular mechanism of DNA excision repair and excision repair maps of the human and E. coli genomes.
- Dynamic maps of UV damage formation and repair.
- Human genome-wide repair map of DNA damage caused by the cigarette smoke carcinogen benzo[a]pyrene.
- Genome-wide transcription-coupled repair in Escherichia coli is mediated by the Mfd translocase.