PUBLICATIONS
Genome-wide Excision Repair in Arabidopsis is coupled to transcription and reflects circadian gene expression patterns.
Plants are exposed to numerous DNA-damaging stresses including the exposure to ultraviolet (UV) component of solar radiation. They employ nucleotide excision repair to remove DNA-bulky adducts and to help eliminate UV-induced DNA lesions, so as to maintain their genome integrity and their fitness. Here, we generated genome-wide single-nucleotide resolution excision repair maps of UV-induced DNA damage in Arabidopsis at different circadian time points. Our data show that the repair of UV lesions for a large fraction of the genome is controlled by the joint actions of the circadian clock and transcription by RNA polymerase II. Our findings reveal very strong repair preference for the transcribed strands of active genes in Arabidopsis, and 10 to 30% of the transcription-coupled repair is circadian time-dependent. This dynamic range in nucleotide excision repair levels throughout the day enables Arabidopsis to cope with the bulky DNA lesion-inducing environmental factors including UV.
- Related:
- Transcription Factors, Nucleotide Excision Repair, and Cancer: A Review of Molecular Interplay
- Dynamics of transcription-coupled repair of cyclobutane pyrimidine dimers and (6-4) photoproducts in Escherichia coli
- 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.
- 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.