Genome-wide CPD repair maps of Caenorhabditis elegans
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ABSTRACT:
PROVIDER: PRJNA1091964 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28462931.fastq.gz | Fastqsanger.gz | |||
| SRR28462932.fastq.gz | Fastqsanger.gz | |||
| SRR28462933.fastq.gz | Fastqsanger.gz | |||
| SRR28462934.fastq.gz | Fastqsanger.gz | |||
| SRR28462935.fastq.gz | Fastqsanger.gz |
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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.
2024-04-02 | GSE262486 | GEO
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:Here, we describe a genome-wide map of photoreactivation repair of UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast (Saccharomyces cerevisiae) by the endogenous yeast CPD photolyase. CPDs were mapped at single nucleotide resolution across the yeast genome using the CPD-seq method immediately after UV radiation (0min) and following 30 or 60min photoreactivation with UVA light. Photoreactivation repair by photolyase was mapped in both wild-type yeast and rad14∆ cells deficient in nucleotide excision repair (NER). We used these data to analyze CPD repair by photolyase in yeast genes, nucleosomes, and transcription factor binding sites.
2025-04-26 | GSE280082 | 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
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Project description:Genome-wide maps of UV damage repair by yeast CPD photolyase
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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.
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Project description:Caenorhabditis elegans is widely used to study DNA repair and related processes such as aging, yet genome-wide nucleotide excision repair remains largely unexplored. Here, we present a comprehensive whole-organism map of UV-induced DNA damage and repair in L1 larvae. Of the two repair pathways - global repair and transcription-coupled repair - global repair predominates, accounting for over 80% of lesion removal; and notably, (6-4) photoproducts are removed by transcription-coupled repair at an extent comparable to CPD, a feature not previously observed in animals. Integration of damage and repair profiles with chromatin features reveals that despite non-uniform damage formation, repair efficiency is the stronger determinant of residual damage. Finally, repair around accessible regions exhibit periodicity, reflecting underlying nucleosome architecture. Together, these findings establish Caenorhabditis elegans as a valuable model organism for interrogating excision repair within a chromatin context and reveal species-specific features that broaden our understanding of DNA repair mechanisms across metazoans.
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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: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.
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Project description:Decline of Nucleotide Excision Repair Capacity in Aged Caenorhabditis elegans
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