Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Yeast Deam-seq

ABSTRACT: Whole genome UV footprinting in yeast using deamination sequencing (Deam-seq), wherein photoproducts induced by high-dose UVB irradiation are revealed as mutations. In Deam-seq, cytosines within cyclobutane pyrimidine dimers (CPDs) are converted to uracil by rapid deamination at elevated temperature. Following CPD repair by photolyase, samples were sequenced at ultra-deep (>7,000×) coverage, enabling calculation of per-base damage fractions (mutant allele frequencies). By comparing cellular and naked DNA, this approach can pinpoint genomic sites bound by proteins that modulate UV damage.

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Saccharomyces cerevisiae

SUBMITTER: Linnéa Ögren

PROVIDER: E-MTAB-15116 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Light-based footprinting of a eukaryotic genome

Project description:Whole genome UV footprinting in yeast using deamination sequencing (Deam-seq), wherein photoproducts induced by high-dose UVC irradiation are revealed as mutations. In Deam-seq, cytosines within cyclobutane pyrimidine dimers (CPDs) are converted to uracil by rapid deamination at elevated temperature. Following CPD repair by photolyase, samples were sequenced at ultra-deep (>7,000×) coverage, enabling calculation of per-base damage fractions (mutant allele frequencies). By comparing cellular and naked DNA, this approach can pinpoint genomic sites bound by proteins that modulate UV damage. The samples were irradiated with UVC on ice, for 45 seconds. Raw fastq files are available in ENA (accession: PRJEB111787).

2026-05-07 | E-MTAB-17008 | biostudies-arrayexpress

Genome-wide maps of UV damage repair by yeast CPD photolyase

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

Major roles of cyclobutane pyrimidine dimers, nucleotide excision repair and ATR in the alternative splicing response to UV irradiation

Project description:Alternative splicing (AS) is the main process that amplifies DNA information and is a crucial target of signaling cascades resulting from UV irradiation of human cells. The specific impact of UV-induced cyclobutane pyrimidine dimers (CPDs) at the transcriptional and AS levels has not been addressed. By using a CPD photolyase, a flavoenzyme that directly reverts CPDs, we analyze the contribution of this lesion to the expression program in human keratinocytes.

2017-04-17 | GSE85510 | GEO

Genome-wide maps of deaminated CPDs (dCPDs) in yeast genomic DNA in vitro

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) genomic DNA that were UV-irradiated and deaminated as naked DNA in vitro. Deaminated CPDs (dCPDs) were mapped at single nucleotide resolution across the yeast genome using the new dCPD-seq method. We used these data to analyze CPD deamination in different trinucleotide sequence contexts.

2025-10-01 | GSE284778 | GEO

Genome-wide maps of deaminated CPDs (dCPDs) following UV-irradiation in cells and deamination as naked DNA in vitro

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

Analysis of UV-induced DNA damage in human cells using CPD-seq 2.0

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

Genome-wide maps of deaminated CPDs (dCPDs) in yeast cells

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

Genome-wide maps of deaminated CPDs (dCPDs) in yeast, biological replicates 2 and 3.

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

Role of Set2 in regulating transcription coupled-nucleotide excision repair

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

Melanoma mutations are caused by deamination of cytosine in pyrimidine dimers

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data