Genome-wide CPD repair maps of Caenorhabditis elegans
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ABSTRACT:
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE262486 | GEO | 2024/04/02
REPOSITORIES: GEO
Similar Datasets
Project description:We have adapted the eXcision Repair-sequencing (XR-seq) method to generate single-nucleotide resolution dynamic repair maps of UV-induced cyclobutane pyrimidine dimers (CPD) photoproducts in the Caenorhabditis elegans (C. elegans) genome. We focus on the C. elegans ortholog of the human XPC-deficient strain (xpc-1) and its exclusive use of transcription-coupled repair. We provide evidence demonstrating the utility of xpc-1 XR-seq as a remarkable tool for detecting nascent transcription and identifying new transcripts. The integration of epigenetic markers, chromatin states, and non-coding RNA annotations supports the robust detection of intergenic nascent transcription by XR-seq. Overall, our results provide a comprehensive view of the transcription-coupled repair landscape in C. elegans, highlighting their potential contributions to our understanding of DNA repair mechanisms and non-coding RNA biology.
2023-11-21 | GSE245181 | GEO
Project description:We developed a method for genome-wide mapping of DNA excision repair named XR-seq (eXcision Repair-seq). Human nucleotide excision repair generates two incisions surrounding the site of damage, creating a ~30-mer. In XR-seq, this fragment is isolated and subjected to high-throughput sequencing. We used XR-seq to produce stranded, nucleotide-resolution maps of repair of two UV-induced DNA damages in human cells, cyclobutane pyrimidine dimers (CPDs) and (6-4) pyrimidine-pyrimidone photoproducts ((6-4)PPs). In wild-type cells, CPD repair was highly associated with transcription, specifically with the template strand. Experiments in cells defective in either transcription-coupled excision repair or general excision repair isolated the contribution of each pathway to the overall repair pattern, and showed that transcription-coupled repair of both photoproducts occurs exclusively on the template strand. XR-seq maps capture transcription-coupled repair at sites of divergent gene promoters and bi-directional eRNA production at enhancers. XR-seq data also uncovered the repair characteristics and novel sequence preferences of CPDs and (6-4)PPs. XR-seq and the resulting repair maps will facilitate studies of the effects of genomic location, chromatin context, transcription, and replication on DNA repair in human cells. We have performed XR-seq for two types of UV-induced damages (CPD and (6-4)PP) in three different cell lines: NHF1, XP-C (XP4PA-SV-EB, GM15983)), and CS-B (CS1ANps3g2, GM16095). Two biological replicates were performed for each experiment, in which independent cell populations were UV treated and subjected to XR-seq.
2015-04-19 | E-GEOD-67941 | biostudies-arrayexpress
Project description:We recently developed a high-resolution genome wide assay for mapping DNA excision repair named eXcision Repair-sequencing (XR-seq) (GEO accession: GSE67941) We have now used this assay to assay the effect of chromatin state on DNA repair. Here we report the results of a time-course of the repair of the UV induced damages cyclobutane pyrimidine dimers (CPDs) and (6-4) pyrimidine-pyrimidone photoproducts [(6-4)PPs] in normal human skin fibroblasts. Comparison of this data to histone modification and DNA-seq maps (ENCODE) revealed initial repair of both damages is enriched in open and active chromatin states, whereas repair in heterochromatic and repressed chromatin states is relatively low and persists to later time points. We performed XR-seq for two types of UV induced damages (CPD and (6-4)PP) at multiple time points after UV irradiation, in normal NHF1, and CS-B (CS1ANps3g2, GM16095) fibroblast cell lines. Two biological replicates were performed for each experiment in which independent independent cell populations were UV treated and subjected to XR-seq. For assaying CPD repair, cells were irradiated with 10J/m2 and for assaying (6-4)PP cells were irradiated with 20J/m2. Raw data for the 1h time points of (6-4)PP repair are the same as in GEO accession GSE67941).
2016-03-15 | E-GEOD-76391 | biostudies-arrayexpress
Project description:We developed a method for genome-wide mapping of DNA excision repair named XR-seq (eXcision Repair-seq). Human nucleotide excision repair generates two incisions surrounding the site of damage, creating a ~30-mer. In XR-seq, this fragment is isolated and subjected to high-throughput sequencing. We used XR-seq to produce stranded, nucleotide-resolution maps of repair of two UV-induced DNA damages in human cells, cyclobutane pyrimidine dimers (CPDs) and (6-4) pyrimidine-pyrimidone photoproducts ((6-4)PPs). In wild-type cells, CPD repair was highly associated with transcription, specifically with the template strand. Experiments in cells defective in either transcription-coupled excision repair or general excision repair isolated the contribution of each pathway to the overall repair pattern, and showed that transcription-coupled repair of both photoproducts occurs exclusively on the template strand. XR-seq maps capture transcription-coupled repair at sites of divergent gene promoters and bi-directional eRNA production at enhancers. XR-seq data also uncovered the repair characteristics and novel sequence preferences of CPDs and (6-4)PPs. XR-seq and the resulting repair maps will facilitate studies of the effects of genomic location, chromatin context, transcription, and replication on DNA repair in human cells.
2015-04-19 | GSE67941 | GEO
Project description:Rad16 is required for global genomic nucleotide excision repair (GG-NER) of UV-induced CPD lesions. Here we have used a novel high-throughput sequencing method known as CPD-seq to map the repair of UV-induced cyclobutane pyrimidine dimers (CPDs) at single nucleotide resolution across the yeast genome in rad16 mutant cells. Analysis of CPD repair indicates that rad16 is generally required for CPD repair in the non-transcribed strand (NTS) of yeast genes and non-transcribed genomic regions.
2019-11-27 | GSE131101 | GEO
Project description:UV-induced DNA lesions are an important contributor to mutagenesis and cancer, but it is not fully understood how the chromosomal landscape influences UV lesion formation and repair. We have used a novel high-throughput sequencing method to precisely map UV-induced cyclobutane pyrimidine dimers (CPDs) at nucleotide resolution throughout the yeast genome. Analysis of CPD formation reveals that nucleosomal DNA having an inward rotational setting is protected from CPD lesions. In strongly positioned nucleosomes, this nucleosome 'photofootprint' overrides intrinsic dipyrimidine sequence preferences for CPD formation. CPD formation is also inhibited by DNA-bound transcription factors, in effect protecting important DNA elements from UV damage. Analysis of CPD repair revealed a clear signature of efficient transcription-coupled nucleotide excision repair. Repair was less efficient at translational positions near a nucleosome dyad and at heterochromatic regions in the yeast genome. These findings define the roles of nucleosomes and transcription factors in UV damage formation and repair. UV mapping data was analyzed for yeast cells irradiated with 125J/m2 and allowed to repair for 0hr (2 samples), 20 minutes, 1 hour, or 2 hours. Data is also included for naked DNA irradiated with UV 60 or 90 J/m2
2016-08-19 | E-GEOD-79977 | biostudies-arrayexpress
Project description:Elf1 is an important transcription elongation factor that has been implicated in transcription coupled-nucleotide excision repair (TC-NER). Here, we have used a high-throughput sequencing method known as CPD-seq to map the repair of UV-induced cyclobutane pyrimidine dimers (CPDs) at single nucleotide resolution across the yeast genome in elf1 mutant cells. Analysis of CPD repair indicates that Elf1 is important for CPD repair in the transcribed strand (TS) of yeast genes, indicating it plays an important role in TC-NER.
2021-04-05 | GSE149082 | GEO
Project description:Here, we describe a new genome-wide map of UV-induced cyclobutane pyrimidine dimers (CPDs) in Drosophila S2 cells and a naked DNA control using CPD-seq. We used this data to analyze CPD formation in nucleosomes and different chromatin states across the Drosophila genome. We analyzed CPD formation alongside existing excision repair-sequencing (XR-seq) data to compare CPD damage and repair rates in five distinct chromatin types in Drosophila. This analysis revealed that CPD repair varied in different chromatin domains, while CPD formation was largely unaffected. Moreover, we observed distinct patterns of repair activity in nucleosomes in different chromatin types.
2024-12-03 | GSE267055 | GEO
Project description:We used a high-throughput sequencing method known as CPD-seq to map the formation of UV-induced cyclobutane pyrimidine dimers (CPD) at single nucleotide resolution in UV-irradiated yeast genomic DNA (naked DNA) in the presence or absence of cytosine methylation at CpG sites by the methyltransferase M.SssI.
2023-08-15 | GSE235068 | GEO
Project description:Nucleotide excision repair is a primary DNA repair mechanism that removes bulky DNA adducts such as UV-induced pyrimidine dimers. Correspondingly, genome-wide mapping of nucleotide excision repair with eXcision Repair sequencing (XR-seq), provides comprehensive profiling of DNA damage repair. A number of XR-seq experiments at a variety of conditions for different damage types revealed heterogenous repair in the human genome. Although human repair profiles were extensively studied, how repair maps vary between primates is yet to be investigated. Here, we characterized the genome-wide UV-induced damage repair maps of the grey mouse lemur,Microcebus murinus, in comparison with human. We derived fibroblast cell lines from mouse lemur and exposed them to UV irradiation. Following repair events were captured genome-wide by XR-seq protocol 1 hour and 5 minutes after irradiation for cyclobutane pyrimidine dimers (CPD) and 6-4 pyrimidine-pyrimidone photoproducts ([6-4]PP), respectively. Mouse lemur repair profiles were analyzed in comparison with the equivalent human fibroblast datasets. We found that transcription-coupled repair levels for CPD repair differs between two primates. Despite this, comparative analysis of human and mouse lemur fibroblasts revealed that genome-wide repair profiles of the homologous regions between the primates are highly correlated. This correlation is stronger for the highly expressed genes as well as the genes sharing high homology. With the inclusion of an additional XR-seq sample derived from another human cell line in the analysis, we found that fibroblasts between two primates repair lesions more similarly relative to two distinct cell lines from human. These results suggest that mouse lemurs and humans, and possibly primates in general, share similar repair mechanism as well as genomic variance distribution.
2020-04-06 | GSE145883 | GEO