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The function of sirtuin family in NER

ABSTRACT: The role of sirtuin family in regulating DNA DSB repair has been extensively investigated, and here, we explore the molecular mechanisms of Sirtuin family in nucleotide excision repair.

ORGANISM(S): Homo Sapiens

SUBMITTER: Zhiyong Mao

PROVIDER: PXD020721 | iProX | Tue Aug 04 00:00:00 BST 2020

REPOSITORIES: iProX

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The deacetylase SIRT6 promotes the repair of UV-induced DNA damage by targeting DDB2.

Geng Anke A Tang Huanyin H Huang Jin J Qian Zhen Z Qin Nan N Yao Yunxia Y Xu Zhu Z Chen Hao H Lan Li L Xie Hongjuan H Zhang Jian J Jiang Ying Y Mao Zhiyong Z

Nucleic acids research 20200901 16

The NAD+-dependent deacetylase and mono-ADP-ribosyl transferase SIRT6 stabilizes the genome by promoting DNA double strand break repair, thereby acting as a tumor suppressor. However, whether SIRT6 regulates nucleotide excision repair (NER) remains unknown. Here, we showed that SIRT6 was recruited to sites of UV-induced DNA damage and stimulated the repair of UV-induced DNA damage. Mechanistic studies further indicated that SIRT6 interacted with DDB2, the major sensor initiating global genome NE ...[more]

PMID: 32789493

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IP-MS/MS analysis of UV induced RPII215 interactome

Project description:Drosophila Melanogaster has been extensively used as a model system to study ionizing radiation and chemical induced mutagenesis, double strand break repair and recombination. However, there are only limited studies on nucleotide excision repair in this important model organism. In this study, we immunopreciptated DNA-directed RNA polymerase II (RPII215) complex from untreated and UV iradiated drosophila S2 cells and identified the protein that interact with it by mass spectrometry.

2022-04-04 | PXD028924 | Pride

Role of Set2 in regulating transcription coupled-nucleotide excision repair

Project description:Role of Set2 in regulating transcription coupled-nucleotide excision repair

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Nucleotide excision repair capacity increases during differentiation of human embryonic carcinoma cells into neurons and muscle cells

Project description:Embryonic stem cells can self-renew and differentiate, holding great promise for regenerative medicine. They also employ multiple mechanisms to preserve the integrity of their genomes. Nucleotide excision repair, a versatile repair mechanism, removes bulky DNA adducts from the genome. However, the dynamics of the capacity of nucleotide excision repair during stem cell differentiation remain unclear. Here, using immunoslot blot assay, we measured repair rates of UV-induced DNA damage during differentiation of human embryonic carcinoma (NTERA-2) cells into neurons and muscle cells. Our results revealed that the capacity of nucleotide excision repair increases as cell differentiation progresses. We also found that inhibition of the apoptotic signaling pathway has no effect on nucleotide excision repair capacity. Furthermore, RNA-seq-based transcriptomic analysis indicated that expression levels of four core repair factors, xeroderma pigmentosum (XP) complementation group A (XPA), XPC, XPG, and XPF-ERCC1, are progressively up-regulated during differentiation, but not those of replication protein A (RPA) and transcription factor IIH (TFIIH). Together, our findings reveal that increase of nucleotide excision repair capacity accompanies cell differentiation, supported by the up-regulated transcription of genes encoding DNA repair enzymes during differentiation of two distinct cell lineages.

2019-03-07 | GSE125370 | GEO

Project description:Mapping nucleotide excision repair without damaged DNA antibody selection

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Integrated multiomic analysis identifies functional epigenetic signatures regulating nucleotide excision repair

Project description:Integrated multiomic analysis identifies functional epigenetic signatures regulating nucleotide excision repair

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

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

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Comparative analysis of genome-wide UV repair events in two primates show different rates but similar distribution.

Project description:Nucleotide excision repair is a primary DNA repair mechanism that removes bulky DNA adducts such as UV-induced pyrimidine dimers. Correspondingly, genome-wide mapping of nucleotide excision repair with eXcision Repair sequencing (XR-seq), provides comprehensive profiling of DNA damage repair. A number of XR-seq experiments at a variety of conditions for different damage types revealed heterogenous repair in the human genome. Although human repair profiles were extensively studied, how repair maps vary between primates is yet to be investigated. Here, we characterized the genome-wide UV-induced damage repair maps of the grey mouse lemur,Microcebus murinus, in comparison with human. We derived fibroblast cell lines from mouse lemur and exposed them to UV irradiation. Following repair events were captured genome-wide by XR-seq protocol 1 hour and 5 minutes after irradiation for cyclobutane pyrimidine dimers (CPD) and 6-4 pyrimidine-pyrimidone photoproducts ([6-4]PP), respectively. Mouse lemur repair profiles were analyzed in comparison with the equivalent human fibroblast datasets. We found that transcription-coupled repair levels for CPD repair differs between two primates. Despite this, comparative analysis of human and mouse lemur fibroblasts revealed that genome-wide repair profiles of the homologous regions between the primates are highly correlated. This correlation is stronger for the highly expressed genes as well as the genes sharing high homology. With the inclusion of an additional XR-seq sample derived from another human cell line in the analysis, we found that fibroblasts between two primates repair lesions more similarly relative to two distinct cell lines from human. These results suggest that mouse lemurs and humans, and possibly primates in general, share similar repair mechanism as well as genomic variance distribution.

2020-04-06 | GSE145883 | GEO

Genome-wide repair maps of nucleotide excision repair in Drosophila and S2 cells.

Project description:We report the application of single-molecule-based sequencing technology (XR-seq) for high-throughput profiling of nucleotide excision repair in Drosophila four developmental stages and S2 cells. By obtaining over six billion bases of sequence from UV and cisplatin damage antibodies immunoprecipitated excision DNA, we generated genome-wide nucleotide excision repair maps of Drosophila Embryo, Larva, Pupa , two gender of adults and S2 cells . We find that Drosophila performs transcription-coupled repair (TCR) at all its developmental stages. S2 cell carry out TCR response to both UV and Cisplatin damage. Finally, we show that XPC repair factor is required for both global and transcription-coupled repair in Drosophila. This study provides the mechanism of nucleotide excision repair of Drosophila in vivo and vitro response to UV and Cisplatin damage.

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Nucleotide Excision Repair Removes Thymidine Analog 5-Ethynyl-2’-deoxyuridine From the Human Genome

Project description:5-Ethynyl-2’-deoxyuridine (EdU) is one of the several thymidine analogs that are used in labeling DNA in cells and in DNA combing (DNA fiber analysis) to study DNA replication1-5. We wished to use these analogs to investigate the repair complex (DNA-protein) of nucleotide excision repair. UV irradiated human cell lines were incubated with EdU, BrdU, IdU, CldU, F-ara-EdU or AmdU to incorporate these analogs into the 26-27 nucleotide long excision repair products. Unexpectedly, we found that EdU even in the absence of DNA damage was released in the form of 26-27nt-long oligomers. We conclude that EdU is incorporated into replicating DNA and is recognized as damage by the nucleotide excision repair system and removed from the genome followed by repair synthesis and re-incorporation into DNA, thus creating futile cycle that leads to cell death. This property of EdU, which was not seen with any of the other thymidine analogs, may be taken advantage of in treating cancer, in particular brain cancers because EdU crosses blood-brain barrier.

2022-08-02 | GSE202784 | GEO

Genome-wide analysis of human global and transcription-coupled excision repair of UV damage at single-nucleotide resolution

Project description:We developed a method for genome-wide mapping of DNA excision repair named XR-seq (eXcision Repair-seq). Human nucleotide excision repair generates two incisions surrounding the site of damage, creating a ~30-mer. In XR-seq, this fragment is isolated and subjected to high-throughput sequencing. We used XR-seq to produce stranded, nucleotide-resolution maps of repair of two UV-induced DNA damages in human cells, cyclobutane pyrimidine dimers (CPDs) and (6-4) pyrimidine-pyrimidone photoproducts ((6-4)PPs). In wild-type cells, CPD repair was highly associated with transcription, specifically with the template strand. Experiments in cells defective in either transcription-coupled excision repair or general excision repair isolated the contribution of each pathway to the overall repair pattern, and showed that transcription-coupled repair of both photoproducts occurs exclusively on the template strand. XR-seq maps capture transcription-coupled repair at sites of divergent gene promoters and bi-directional eRNA production at enhancers. XR-seq data also uncovered the repair characteristics and novel sequence preferences of CPDs and (6-4)PPs. XR-seq and the resulting repair maps will facilitate studies of the effects of genomic location, chromatin context, transcription, and replication on DNA repair in human cells. We have performed XR-seq for two types of UV-induced damages (CPD and (6-4)PP) in three different cell lines: NHF1, XP-C (XP4PA-SV-EB, GM15983)), and CS-B (CS1ANps3g2, GM16095). Two biological replicates were performed for each experiment, in which independent cell populations were UV treated and subjected to XR-seq.

2015-04-19 | E-GEOD-67941 | biostudies-arrayexpress

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