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UVDE-seq mapping of UV-induced 6-4PPs and atypical TA photoproducts

ABSTRACT: 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).

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE190471 | GEO | 2023/02/28

REPOSITORIES: GEO

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UVDE-HS-seq mapping of UV-induced 6-4PPs and atypical TA photoproducts

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).

2023-02-28 | GSE214217 | GEO

CPD-seq mapping of UV damage repair in rad16 mutant yeast

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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Global Genome-Nucleotide Excision Repair is Organised into Domains Promoting Efficient DNA Repair in Chromatin

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

Elf1 promotes TC-NER in yeast by using its C-terminal domain to bind TFIIH

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

UVDE-seq mapping of UV-induced non-CPD lesions

Project description:Here we have used a novel high-throughput sequencing method known as UVDE-seq to map the formation of non-CPD lesions at single nucleotide resolution across the yeast genome in wild-type and rad16 mutant cells, which are deficient in GG-NER.

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The yeast GG-NER complex evicts histone H2A.Z-containing barrier nucleosomes from CID boundaries during DNA repair

Project description:Background: Repair of DNA damage requires chromatin remodeling to permit removal of the lesions. How nucleosomes are remodelled to initiate repair of DNA damage remains largely unknown. Here, we describe how chromatin is altered during repair of UV-induced DNA damage at the level of the linear organisation of nucleosomes. Results: Using MNase-seq, we identified a subset of nucleosomes in the genome that are remodelled in UV-damaged wild-type yeast cells. We mapped the genomic location of these nucleosomes, showing that they contain the histone variant H2A.Z. The remodelling observed is consistent with histone exchange or eviction at these positions. This depends on the yeast SWI/SNF global genome nucleotide excision repair (GG-NER) chromatin-remodelling complex. Remarkably, we found that in the absence of DNA damage, the GG-NER complex occupies chromatin at nucleosome free regions separating adjacent nucleosomes. This establishes the nucleosome structure at these genomic locations, which we refer to as GG-NER complex binding sites (GCBS’s). We observed that these sites are frequently located precisely at certain boundary regions that delineate chromasomally interacting domains (CIDs). These boundaries define chromosomal domains of higher-order nucleosome-nucleosome interaction. We demonstrate that the GG-NER complex redistributes following remodelling of these nucleosomes after DNA damage taking up genomic positions located within the CIDs. This permits the efficient removal of DNA damage at these sites. Conclusions: We argue that organising DNA repair in the genome as described may define origins of DNA repair that greatly reduces the genomic search space for DNA damage recognition, thus ensuring the efficient repair of damage in chromatin.

2018-12-06 | E-MTAB-6569 | biostudies-arrayexpress

UVDE-seq mapping of UV-induced 6-4PPs and atypical TA photoproducts

Project description:UVDE-seq mapping of UV-induced 6-4PPs and atypical TA photoproducts

| PRJNA787240 | ENA

UVDE-HS-seq mapping of UV-induced 6-4PPs and atypical TA photoproducts

Project description:UVDE-HS-seq mapping of UV-induced 6-4PPs and atypical TA photoproducts

| PRJNA884390 | ENA

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

Role of H3K36 methylation in regulating transcription coupled-nucleotide excision repair

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

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