Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA341681 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4124890.fastq.gz | Fastqsanger.gz | |||
| SRR4124891.fastq.gz | Fastqsanger.gz | |||
| SRR4124892.fastq.gz | Fastqsanger.gz | |||
| SRR4124893.fastq.gz | Fastqsanger.gz | |||
| SRR4124894.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 7 |
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Project description:A genome-wide study reveals a pathway for small RNA-mediated recognition of UV-induced DNA lesions (smallRNAs)
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Project description:A genome-wide study reveals a pathway for small RNA-mediated recognition of UV-induced DNA lesions
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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
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: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: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:If the genome contains outlier sequences extraordinarily sensitive to environmental agents, these would be sentinels for monitoring personal carcinogen exposure and might drive direct changes in cell physiology rather than acting through rare mutations. New methods, adductSeq and freqSeq, provided statistical resolution to quantify rare lesions at single-base resolution across the genome. Primary human melanocytes, but not fibroblasts, carried spontaneous apurinic sites and TG sequence lesions more frequently than UV-induced cyclobutane pyrimidine dimers (CPDs). UV exposure revealed hyperhotspots acquiring CPDs up to 170 fold more frequently than the genomic average; these sites were more prevalent in melanocytes. Hyperhotspots were disproportionately located near genes, particularly for RNA-binding proteins, with the most-recurrent hyperhotspots at a fixed position within two motifs: one occurring at ETS1 transcription factor binding sites, known to be UV targets, and at sites of mTOR/TOP-tract translation regulation; the second occurring at A2-15TTCTY, which developed "dark CPDs" after UV exposure, repaired CPDs slowly, and had accumulated CPDs prior to the experiment. Motif locations active as hyperhotspots differed between cell types. Melanocyte CPD hyperhotspots aligned precisely with recurrent UV signature mutations in individual gene promoters of melanomas and with known cancer drivers. At sunburn levels of UV exposure, every cell would have a hyperhotspot CPD in each of the ~20 targeted cell pathways, making hyperhotspots act as epigenetic marks. Purpose: These experiments searched for genomic sites in human primary fibroblasts and melanocytes that are extraordinarily sensitive to DNA damage, primarily cyclobutane pyrimidine dimers (CPDs) induced by UVC or UVB radiation. They separately detected abasic sites and other spontaneous DNA damage when present.
2020-04-14 | GSE137226 | GEO
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 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: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