PUBLICATIONS
Human genome-wide repair map of DNA damage caused by the cigarette smoke carcinogen benzo[a]pyrene.
Benzo[a]pyrene (BaP), a polycyclic aromatic hydrocarbon, is the major cause of lung cancer. BaP forms covalent DNA adducts after metabolic activation and induces mutations. We have developed a method for capturing oligonucleotides carrying bulky base adducts, including UV-induced cyclobutane pyrimidine dimers (CPDs) and BaP diol epoxide-deoxyguanosine (BPDE-dG), which are removed from the genome by nucleotide excision repair. The isolated oligonucleotides are ligated to adaptors, and after damage-specific immunoprecipitation, the adaptor-ligated oligonucleotides are converted to dsDNA with an appropriate translesion DNA synthesis (TLS) polymerase, followed by PCR amplification and next-generation sequencing (NGS) to generate genome-wide repair maps. We have termed this method translesion excision repair-sequencing (tXR-seq). In contrast to our previously described XR-seq method, tXR-seq does not depend on repair/removal of the damage in the excised oligonucleotides, and thus it is applicable to essentially all DNA damages processed by nucleotide excision repair. Here we present the excision repair maps for CPDs and BPDE-dG adducts generated by tXR-Seq for the human genome. In addition, we report the sequence specificity of BPDE-dG excision repair using tXR-seq.
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- UV-induced reorganization of 3D genome mediates DNA damage response
- Global repair is the primary nucleotide excision repair subpathway for the removal of pyrimidine-pyrimidone (6-4) damage from the Arabidopsis genome
- The interplay of 3D genome organization with UV-induced DNA damage and repair
- The Mfd protein is the Transcription-Repair Coupling Factor (TRCF) in Mycobacterium smegmatis
- Effects of replication domains on genome-wide UV-induced DNA damage and repair
- 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.
- Genome-wide transcription-coupled repair in Escherichia coli is mediated by the Mfd translocase.