Photodamage repair pathways contribute to the accurate maintenance of DNA methylome landscape upon UV exposure
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PROVIDER: PRJNA548919 | ENA |
REPOSITORIES: ENA
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Project description:We report the methylation level of photodamage repair deficient plants 24h upon UV-C exposure. We determined the methlome changes genome wide and at photodamaged sites using NGS approaches.
2019-11-01 | GSE132750 | GEO
Project description: Not available
| S-EPMC6886878 | biostudies-literature
Project description:This project was conducted by Nitin S. Baliga of the Halobacterium group at the Institute for Systems Biology in collaboration with Jocelyne Diruggiero of University of Maryland. Halobacterium NRC-1 cell pellets were resuspended in an isotonic buffer at a low density, placed on ice and exposed to 200J/m2 of UV-C irradiation, returned to the growth medium and allowed to recover at 42oC in dark (D) or light (L). Total RNA was collected from each sample at 30 minutes (D30 and L30) and 60 minutes (L60 and D60). The control (C) was processed in a manner to identical to L60 except that it did not suffer any UV-C insult. The reference RNA was prepared from an aliquot of the same culture just prior to UV-C irradiation. Therefore the reference was also exposed to initial perturbations prior to UV-C irradiation such as change of growth medium to buffer and change of temperature from 42oC to ice. Keywords = ISB Keywords = Halobacterium NRC-1 Keywords = UV repair Keywords = ultraviolet radiation Keywords = stress response Keywords: other
2004-02-14 | GSE1040 | 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: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.
2016-08-19 | GSE79977 | GEO
Project description:UV-induced DNA damage is the major carcinogen of skin cancer. We developed HS-Damage-seq to map UV damage with unprecedented sensitivity and resolution in human cells. While the distribution of UV-induced damage are mainly determined by sequence context and essentially uniform throughout the genome, transcription factors can affect damage formation at specific positions. With time-course experiments, we observed changes in damage distribution at particular genomic loci and chromatin states, which reflects the nucleotide excision repair preferences and complements the repair maps by XR-seq. Our results demonstrated that while initial damage is uniformly distributed, they are heterogeneously repaired throughout the genome. The combination of damage and repair maps provides a holistic perspective of UV damage and repair in the human genome.
2017-06-27 | GSE98025 | 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:We recently developed high-throughput sequencing approaches, eXcision Repair sequencing (XR-seq) and Damage-seq, to generate genome-wide mapping of DNA damage formation and excision repair, respectively, with single-nucleotide resolution. Here, we adopted time-course XR-seq data to profile UV-induced excision repair dynamics, paired with Damage-seq data to quantify the overall induced DNA damage. We identified genome-wide repair hotspots that are subject to exemplified amount of repair very soon after UV irradiation. We show that such repair hotspots do not result from hypersensitivity to DNA damage and are thus not damage hotspots. We find that the earliest repair occur preferentially in promoters and enhancers from open-chromatin regions. The repair hotspots are also significantly enriched for frequently interacting regions and super-enhancers, both of which are hotspots for local chromatin interactions. We further extend the interrogation of chromatin organization to DNA replication timing and conclude that early-repair hotspots are enriched for early-replication domains. Collectively, we report genome-wide early-repair hotspots of UV-induced damage, in association with chromatin states and epigenetic compartmentalization of the human genome.
2020-04-09 | GSE148303 | GEO
Project description:In this study, we performed integrative multi-omics studies to understand the complex mechanisms underlying UV photobiological effects. While H3K27ac and genetic mutations can both contribute to UV-induced transcriptomic changes, additional omics-based studies on other histone modifications, DNA methylation, and whole genome mapping of genetic mutations will provide a thorough understanding of UV-gene interactions in skin disease pathogenesis. The new UV target genes that we identified have important clinical implications in skin carcinogenesis..
2017-04-11 | GSE97577 | GEO
Project description:af09_lignin - dml6 - Transcriptome analysis of lignin mutants and UV stress effect on secondary wall synthesis - DML6 vs S DML6+UV vs S+UV S vs S+UV DML6 vs DML6+UV Keywords: normal vs disease comparison,treated vs untreated comparison
2007-06-20 | GSE8094 | GEO