Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1168543 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30874416_1.fastq.gz | Fastqsanger.gz | |||
| SRR30874416_2.fastq.gz | Fastqsanger.gz | |||
| SRR30874417_1.fastq.gz | Fastqsanger.gz | |||
| SRR30874417_2.fastq.gz | Fastqsanger.gz | |||
| SRR30874418_1.fastq.gz | Fastqsanger.gz |
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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.
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Project description:Repair of UV damage from the transcribed strand (TS) of yeast genes is rapid due to the transcription coupled nucleotide excision repair (TC-NER) pathway. TC-NER is triggered when RNA polymerase stalls at UV damage, such as a UV-induced cyclobutane pyrimidine dimer (CPD). During transcription, the histone methyltransferase Set2 methylates histone H3K36, but it is not known if Set2 regulates TC-NER. Here, we report genome-wide repair maps of UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast cells lacking Set2.
2022-02-21 | GSE179794 | GEO
Project description:We characterized the role of H3K36 methylation in regulating repair of UV damage from the transcribed strand (TS) of yeast genes by the transcription coupled nucleotide excision repair (TC-NER) pathway. TC-NER is triggered when RNA polymerase stalls at UV damage, such as a UV-induced cyclobutane pyrimidine dimer (CPD). During transcription, the histone methyltransferase Set2 methylates histone H3K36, but it is not known if H3K36 methylation regulates TC-NER. Here, we report genome-wide repair maps of UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast cells containing mutants in histone H3K36 (or set2).
2022-02-21 | GSE194101 | GEO
Project description:The mammalian genome is constantly exposed to genotoxins that can lead to mutations and ultimately tumorigenesis. Despite cancer being recognized as a genetic disease, much is still unknown regarding tumor induction and evolution of the cancer genome. To study gradual (reactive oxygen species, ROS) and acute (ultraviolet radiation, UV) mutagenic processes both in vitro and then in vivo, we first use microfluidic separation of cells after a single mitosis following pulse mutagenesis. While UV mutations tend to be fixed after one cell cycle and show mirror image mutation patterns between sister cells from a single mitosis, ROS mutations do not. We next show that while both ROS and UV mutation rates are reduced as a function of transcription, only UV has a strand-specific repair signature. Lastly, we resolve pulse induced lesion segregation to single haplotypes by analysing liver tumour genomes from F1 mice treated with N-nitroso-diethylamine (DEN). In summary, we have established highly controlled systems to study 3 distinct forms of mutagenesis at their inception in mammalian cells, providing insights into how these mutations are fixed at the genome scale.
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Project description:We used a novel high-throughput sequencing method known as UVDE-HS-seq to map the formation of UV-induced 6-4 photoproducts (6-4PP) and atypical thymidine-adenine (TA) photoproducts at single nucleotide resolution across the yeast genome in wild-type cells. We also analyzed 6-4PP and TA photoproducts in UV-irradiated yeast genomic DNA (i.e., naked DNA).
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Project description:Nucleosomes are a significant barrier to the repair of UV damage because they impede damage recognition by nucleotide excision repair (NER). The RSC chromatin remodeler functions in cells to promote DNA access by moving or evicting nucleosomes and has been linked to NER in yeast. Here, we report genome-wide repair maps of UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast cells lacking Rsc2.
2021-04-12 | GSE168369 | 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.
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Project description:We used a novel high-throughput sequencing method known as UVDE-seq to map the formation of UV-induced 6-4 photoproducts (6-4PP) and atypical thymidine-adenine (TA) photoproducts at single nucleotide resolution across the yeast genome in wild-type and rad16 mutant cells, which are deficient in GG-NER. We also analyzed 6-4PP and TA photoproducts in UV-irradiated yeast genomic DNA (i.e., naked DNA).
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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