Similar Datasets
Project description:XR-seq was performed to map the repair of UV-induced photoproducts.
2024-10-30 | GSE280349 | GEO
Project description:(6-4)PP and CPD Damage-seq data for L1 stage wildtype, csb-1 and xpc-1 C.elegans
| PRJNA1177895 | ENA
Project description:RNA-seq analysis was conducted to quantify the gene expression levels in each strain.
2024-10-30 | GSE280348 | GEO
Project description:RNA-seq for L1 stage wildtype, csb-1 and xpc-1 C.elegans
| PRJNA1177893 | ENA
Project description:UV-induced (6-4)PP and CPD XR-seq data for L1 stage wildtype, csb-1 and xpc-1 C.elegans
| PRJNA1177894 | ENA
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. An early study reported that Drosophila lacks the transcription-coupled repair (TCR) form of nucleotide excision repair. This conclusion was seemingly supported by the Drosophila genome sequencing project, which revealed that Drosophila lacks a homolog to CSB, which is known to be required for TCR in mammals and yeasts. However, by using excision repair sequencing (XR-seq) genome-wide repair mapping technology, we recently found that the Drosophila S2 cell line performs TCR comparable to human cells. Here, we have extended this work to Drosophila at all its developmental stages. We find TCR takes place throughout the life cycle of the organism. Moreover, we find that in contrast to humans and other multicellular organisms previously studied, the XPC repair factor is required for both global and transcription-coupled repair in Drosophila.
| S-EPMC8892495 | biostudies-literature
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:Nucleotide excision repair removes UV-induced DNA damage through two distinct sub-pathways, global repair and transcription-coupled repair (TCR). Numerous studies have shown that in human and other mammalian cell lines that the XPC protein is required for repair of DNA damage from nontranscribed DNA via global repair and the CSB protein is required for repair of lesions from transcribed DNA via TCR. Therefore, it is generally assumed that abrogating both sub-pathways with an XPC-/-/CSB-/- double mutant would eliminate all nucleotide excision repair. Here we describe the construction of three different XPC-/-/CSB-/- human cell lines that, contrary to expectations, perform TCR. The XPC and CSB genes were mutated in cell lines derived from Xeroderma Pigmentosum patients as well as from normal human fibroblasts and repair was analyzed at the whole genome level using the very sensitive XR-seq method. As predicted, XPC-/- cells exhibited only TCR and CSB-/- cells exhibited only global repair. However, the XPC-/-/CSB-/- double mutant cell lines, although having greatly reduced repair, exhibited TCR. Mutating the CSA gene to generate a triple mutant XPC-/-/CSB-/-/CSA-/- cell line eliminated all residual TCR activity. Together, these findings provide new insights into the mechanistic features of mammalian nucleotide excision repair.
| S-EPMC10325923 | biostudies-literature
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
Project description:Expression profiles of AhR mutant vs N2 wild-type C.elegans, in L1 larval stage compared by using 23232 feature WUSTL microarray
2009-12-19 | GSE16036 | GEO