UVDE-seq mapping of UV-induced non-CPD lesions
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ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
PROVIDER: GSE144679 | GEO | 2020/11/19
REPOSITORIES: GEO
Similar Datasets
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:Elf1 is an important transcription elongation factor that has been implicated in transcription coupled-nucleotide excision repair (TC-NER). Here, we have used a 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 elf1 mutant cells. Analysis of CPD repair indicates that Elf1 is important for CPD repair in the transcribed strand (TS) of yeast genes, indicating it plays an important role in TC-NER.
2021-04-05 | GSE149082 | 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: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).
2023-02-28 | GSE190471 | GEO
Project description:Transcription coupled-nucleotide excision repair (TC-NER) repairs DNA lesions that stall RNA polymerase II (Pol II) transcription. Here, we show that the C-terminal domain (CTD) of elongation factor-1 (Elf1) plays a critical role in TC-NER in yeast. Analysis of genome-wide repair of UV-induced cyclobutane pyrimidine dimers (CPDs) using CPD-seq indicates that the Elf1 CTD is required for efficient Rad26-dependent and Rad26-independent TC-NER across the yeast genome. The Elf1-CTD is also important for TC-NER in rad16∆ cells deficient in GG-NER. Finally, we show that a mutant in the Elf1-CTD (elf1-Y99A) that disrupts binding to a subunit of TFIIH affects Rad26-independent repair in a rad26∆ mutant background.
2024-05-31 | GSE243603 | 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.
2016-08-19 | GSE79977 | GEO
Project description:The rates at which lesions are removed by DNA repair can vary widely throughout the genome with important implications for genomic stability. We measured the distribution of nucleotide excision repair (NER) rates for UV induced lesions throughout the yeast genome. By plotting these repair rates in relation to all ORFs and their associated flanking sequences, we reveal that in normal cells, genomic repair rates display a distinctive pattern, suggesting that DNA repair is highly organised within the genome. We compared genome-wide DNA repair rates in wild type and in RAD16 deleted cells, which are defective in the global genome-NER (GG-NER) sub-pathway, demonstrating how this alters the normalâ¨distribution of NER rates throughout the genome. We examine the genomic locations of global genome NER factor binding in chromatin before and after UV irradiation, and reveal that GG-NER is organized and initiated from specific locations. By controlling the chromatin occupancy of the histone acetyl transferase Gcn5, the GG-NER complex regulates the histone H3 acetylation status and chromatin structure in the vicinity of these genomic sites to promote the efficient DNA repair of UV induced lesions. This demonstrates that chromatin remodeling during the GG-NER process is organized into domains in the genome. Importantly, we demonstrate that deleting the histone modifier GCN5, an accessory factor required for chromatin remodeling during GG-NER, significantly alters the genomic distribution of NER rates. These observations could have important implications for the effect of histone and chromatin modifiers on the distribution of genomic mutations acquired throughout the genome.
2016-07-21 | E-MTAB-4641 | biostudies-arrayexpress
Project description:UVDE-seq mapping of UV-induced non-CPD lesions
| PRJNA604574 | ENA
Project description:CPD-seq mapping of UV damage repair in rad16 mutant yeast
| PRJNA542684 | ENA
Project description:UV light is an initiating factor in the etiology of human melanoma due to its production of mutagenic DNA photoproducts, primarily cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts. UV-induced mutations are heterogeneously distributed across melanoma genomes, being enriched, for example, in regions of compact heterochromatin and at active transcription factor binding sites (TFBS). Differential ability of nucleotide excision repair (NER) to remove UV-induced DNA lesions in these regions has been proposed as the primary factor establishing the observed regional differences in melanoma mutation density. However, it is not fully understood to what extent the binding of transcription factors and chromatin structure affect UV damage formation, nor how variations in initial damage levels contribute to mutagenesis. Here, we directly mapped sites of CPD formation across the genome in human cells, and show that variations in UV damage formation, due to primary chromatin structure and transcription factor binding, are strongly correlated with local differences in melanoma mutation density. Analysis of individual transcription factors revealed that the E26 transformation-specific (ETS) family is the major contributor to increased somatic mutation density at TFBS in melanoma, primarily because DNA binding by ETS family transcription factors stimulates the formation of CPD lesions, generating UV damage 'hotspots'. Moreover, many ETS binding sites, including those associated with known cancer genes, are recurrently mutated in human melanomas. These findings establish variable lesion formation as a key contributor to mutation heterogeneity in cancer.
2018-06-21 | GSE103487 | GEO