Genome-wide maps of deaminated CPDs (dCPDs) in yeast genomic DNA in vitro
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ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
PROVIDER: GSE284778 | GEO | 2025/10/01
REPOSITORIES: GEO
Similar Datasets
Project description:Here, we describe a genome-wide map of uracil lesions arising from deaminated UV-induced cyclobutane pyrimidine dimers (CPDs) that arose from UV irradiation of yeast cells (Saccharomyces cerevisiae) and deamination in vitro as isolated yeast genomic DNA (i.e., naked DNA control). Deaminated CPDs (dCPDs) were mapped at single nucleotide resolution across the yeast genome using the new dCPD-seq method in repair-deficient (rad14∆), G2/M-arrested (cdc13-1) yeast cells immediately after UV irradiation (0 hour) and following 6 hour (6hr), 24hr, or 48hr of deamination in solution in vitro. We also generated a full deamination control, in which genomic DNA from a 48h deamination sample was incubated in vitro for an additional 16h at 67C. We used these data to analyze CPD deamination in different trinucleotide sequence contexts, yeast genes, transcription factor binding sites, and nucleosomes.
2025-10-01 | GSE285152 | GEO
Project description:Here, we describe a genome-wide map of uracil lesions arising form deaminated UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast (Saccharomyces cerevisiae). Deaminated CPDs (dCPDs) were mapped at single nucleotide resolution across the yeast genome using the new dCPD-seq method in repair-deficient (rad14∆), G2/M-arrested (cdc13-1) yeast cells immediately after UV irradiation (0 hour) and following 6 hour (6hr), 24hr or 48hr of deamination in arrested, repair-deficient yeast cells. We used these data to analyze CPD deamination in different trinucleotide sequence contexts, yeast genes, transcription factor binding sites, and nucleosomes.
2025-10-01 | GSE284099 | GEO
Project description:Here, we describe a genome-wide map of uracil lesions arising form deaminated UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast (Saccharomyces cerevisiae). Deaminated CPDs (dCPDs) were mapped at single nucleotide resolution across the yeast genome using the new dCPD-seq method in repair-deficient (rad14∆), G2/M-arrested (cdc13-1) yeast cells immediately after UV irradiation (0 hour) and following 6 hour (6hr), 24hr, or 48hr of deamination in arrested, repair-deficient yeast cells. We also generated a full deamination control, in which genomic DNA from a 48h cellular deamination sample was incubated in vitro for an additional 16h at 67C. We used these data to analyze CPD deamination in different trinucleotide sequence contexts, yeast genes, transcription factor binding sites, and nucleosomes.
2025-10-01 | GSE285153 | GEO
Project description:The majority of sunlight-associated melanomas carry a unique UV-related C to T mutation signature at dipyrimidine sites. UVB radiation is known to induce cyclobutane pyrimidine dimers (CPDs) as the major form of DNA damage, but the mechanism of how these DNA lesions lead to mutations is unknown. To map the genome-wide distribution of CPDs at single base resolution, we developed a new method, circle damage sequencing (circle-damage-seq). We found that in human cells CPDs form in a specific tetranucleotide sequence context (5’PyPy<>PyT/A), but this alone does not explain the mutation patterns. To test whether mutations arise at CPDs by cytosine deamination, we next applied a modification of circle-damage-seq and mapped UVB-induced cytosine-deaminated CPDs. We observed that the transcription start sites (TSS) are the sequences most protected from CPDs and deaminated CPDs. The strongest spike of CPDs and deaminated CPD lesions was found immediately upstream of the TSS, suggesting a mutation-promoting role of bound transcription factors. Most significantly, the genome-wide dinucleotide and trinucleotide sequence specificity of deaminated CPDs matched the prominent mutation signature found in melanomas. Our data identifies the cytosine-deaminated CPD as the leading premutagenic lesion responsible for the vast majority of mutations in sun-exposure-linked melanomas.
2020-10-22 | GSE159807 | 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:Noncoding mutation hotspots have been identified in melanoma and many of them occur at the binding sites of E26 transformation-specific (ETS) proteins; however, their formation mechanism and functional impacts are not fully understood. Here, we used UV damage sequencing data and analyzed cyclobutane pyrimidine dimer (CPD) formation, DNA repair, and CPD deamination in human cells at single-nucleotide resolution. Our data shows prominent CPD hotspots immediately after UV irradiation at ETS binding sites, particularly at sites with a conserved TTCCGG motif, which correlate with mutation hotspots identified in cutaneous melanoma. Additionally, CPDs are repaired slower at ETS binding sites than in flanking DNA. Cytosine deamination in CPDs to uracil is suggested as an important step for UV mutagenesis. However, we found that CPD deamination is significantly suppressed at ETS binding sites, particularly for the CPD hotspot on the 5’ side of the ETS motif, arguing against a role for CPD deamination in promoting ETS-associated UV mutations. Finally, we analyzed a subset of frequently mutated promoters, including the ribosomal protein genes RPL13A and RPS20, and found that mutations in the ETS motif can significantly reduce the promoter activity. Thus, our data identifies high UV damage and low repair, but not CPD deamination, as the main mechanism for ETS-associated mutations in melanoma and uncover new roles of often-overlooked mutation hotspots in perturbing gene transcription.
2023-12-01 | GSE235483 | 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: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: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: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