Ontology highlight
ABSTRACT:
PROVIDER: PRJEB44262 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Primordial germ cell DNA demethylation and development require DNA translesion synthesis
| PRJNA1068075 | ENA
Project description:The NuA4 complex promotes Translesion Synthesis (TLS) - mediated DNA damage tolerance
| PRJNA276018 | ENA
Project description:Benzo[a]pyrene (BaP), a polycyclic aromatic hydrocarbon, is the major cause of lung cancer. It forms covalent DNA adducts after metabolic activation and induces mutations. We have developed a method capturing oligonucleotides carrying bulky base adducts, including UV-induced cyclobutane pyrimidine dimers (CPDs) and BaP diol epoxide-deoxyguanosine (BPDE-dG), which are removed from the genome by nucleotide excision repair. The isolated oligonucleotides are ligated to adaptors and after damage-specific immunoprecipitation the adaptor-ligated oligonucleotides are converted to dsDNA with an appropriate translesion DNA synthesis (TLS) polymerase followed by PCR amplification and next-generation sequencing (NGS) to generate genome-wide repair maps. We have named this method as translesion eXcision Repair-sequencing (tXR-seq). In contrast to our previously described XR-seq method, the tXR-seq does not depend on repair/removal of the damage in the excised oligonucleotides and hence it is applicable to essentially all DNA damages processed by nucleotide excision repair. Here, we present the excision repair maps for CPDs and BPDE-dG adducts generated by tXR-Seq for the human genome. Additionally, we observe novel sequence specificity of BPDE-dG excision repair by using tXR-seq.
2017-06-12 | GSE97675 | GEO
Project description:Translesion DNA synthesis-driven mutagenesis in very early embryogenesis of fast cleaving embryos
| PRJNA677917 | ENA
Project description:Antimicrobial-induced DNA damage, and subsequent repair via upregulation of DNA repair factors, including error-prone translesion polymerases, can lead to the increased accumulation of mutations in the microbial genome, and ultimately increased risk of acquired mutations associated with antimicrobial resistance. While this phenotype is well described in bacterial species, it is less thoroughly investigated amongst microbial fungi. Here, we monitor DNA damage induced by antifungal agents in the fungal pathogen Candida albicans, and find that commonly used antifungal drugs are able to induce DNA damage, leading to the upregulation of transcripts encoding predicted error-prone polymerases and related factors. We focus on REV1, encoding a putative error-prone polymerase, and find that while deleting this gene in C. albicans leads to increased sensitivity to DNA damage, it also unexpectedly renders cells more likely to incur mutations and evolve resistance to antifungal agents. We further find that deletion of REV1 leads to a significant depletion in the uncharacterized protein Shm1, which itself plays a role in fungal mutagenesis. Together, this work lends new insight into previously uncharacterized factors with important roles in the DNA damage response, mutagenesis, and the evolution of antifungal drug resistance.
2025-05-07 | PXD055008 | Pride
Project description:The cGAS-cGAMP-STING pathway is crucial for antiviral immunity. While cytosolic cGAS detects viral DNA, most DNA viruses shield their genome and invade the nucleus, where chromatin restricts cGAS activation. How viruses may activate nuclear cGAS is not well understood. Here, we show that several herpesvirus proteins trigger nuclear cGAS activation by perturbing centromeres, where cGAS is enriched. The herpes simplex virus type 1 (HSV-1) ubiquitin ligase ICP0, which degrades centromeric proteins, promotes centromeric DNA amplification through the translesion DNA synthesis (TLS) pathway in quiescent monocyte-derived cells, thereby activating nuclear cGAS. During infection, HSV-1 evades this detection by also expressing UL36USP, a suppressor of TLS. Similarly to ICP0, the cytomegalovirus IE1 protein causes centromeric DNA amplification and cGAS activation. We define this mechanism as Viral-Induced Centromeric DNA Amplification and Recognition (VICAR), uncovering a non-mitotic, immune-activating role of centromeres.
2025-05-25 | GSE254979 | GEO