Zuo1 supports G4 structure formation and directs repair towards nucleotide excision repair
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ABSTRACT:
PROVIDER: PRJNA628932 | ENA |
REPOSITORIES: ENA
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Project description:Nucleic acids can fold into G-quadruplex (G4) structures that can fine tune biological processes. Proteins are required to recognize G4 structures and coordinate their function. We identify Zuo1 as a novel G4-binding protein in a yeast one-hybrid screen. Biochemical and molecular experiments in yeast confirm that Zuo1 specifically binds to G4 structures in vitro and in vivo. In vivo in the absence of Zuo1 less G4 structures form, cell growth slows and cells become UV sensitive. Subsequent experiments reveal that these cellular changes are due to reduced levels of G4 structures. Interestingly, Zuo1 function and binding to G4 structures results in the recruitment of nucleotide excision repair (NER) factors, which has a positive effect on genome stability. Cells lacking functional NER as well as Zuo1 accumulate G4s structures, which become accessible for translesion synthesis. Our results suggest a model in which Zuo1 supports NER function and regulates the choice of the DNA repair pathway near G4 structures.
2020-06-23 | GSE149502 | GEO
Project description: Not available
| S-EPMC7413387 | biostudies-literature
Project description:Ribonucleotide excision repair prevents intestinal tumorigenesis
| PRJNA436583 | ENA
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.
2022-02-25 | GSE184926 | GEO
Project description:Transcriptional analysis of nucleotide excision repair defects
| PRJNA714383 | ENA
Project description:In the bacterium Escherichia coli, RecG directs DNA synthesis during the repair of DNA double-strand breaks by homologous recombination. Examination of RecA binding during double-strand break repair in Escherichia coli in the presence and absence of RecG protein
2016-05-19 | E-GEOD-77181 | biostudies-arrayexpress
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
Project description:We are investigating the transcriptional response of yeast to modulation of the expression of base excision repair players, these generate different dna lesions of abasic sites of strand breaks; We used microarrays to detail the global programme of gene expression underlying the DNA damage response in yeast Experiment Overall Design: Yeaststrains with different expression levels of players in base excision repair (in biological triplicate) were grown to mid log phase. The expression responses were compared to each other and we have deciphered a gene expression profile that is specific for DNA damage in yeast.
2008-06-16 | E-GEOD-9295 | biostudies-arrayexpress
Project description:Lamin A/C promotes DNA base excision repair
| PRJNA512097 | ENA
Project description:We recently developed high-throughput sequencing approaches, eXcision Repair sequencing (XR-seq) and Damage-seq, to generate genome-wide mapping of DNA damage formation and excision repair, respectively, with single-nucleotide resolution. Here, we adopted time-course XR-seq data to profile UV-induced excision repair dynamics, paired with Damage-seq data to quantify the overall induced DNA damage. We identified genome-wide repair hotspots that are subject to exemplified amount of repair very soon after UV irradiation. We show that such repair hotspots do not result from hypersensitivity to DNA damage and are thus not damage hotspots. We find that the earliest repair occur preferentially in promoters and enhancers from open-chromatin regions. The repair hotspots are also significantly enriched for frequently interacting regions and super-enhancers, both of which are hotspots for local chromatin interactions. We further extend the interrogation of chromatin organization to DNA replication timing and conclude that early-repair hotspots are enriched for early-replication domains. Collectively, we report genome-wide early-repair hotspots of UV-induced damage, in association with chromatin states and epigenetic compartmentalization of the human genome.
2020-04-09 | GSE148303 | GEO