Caenorhabditis elegans
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-21467
PROVIDER: PRJNA125817 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The nematode Caenorhabditis elegans has been used extensively to study responses to DNA damage. In contrast, little is known about DNA repair in this organism. C. elegans is unusual in that it encodes few DNA glycosylases and the uracil-DNA glycosylase (UDG) encoded by the ung-1 gene is the only known UDG. C. elegans could therefore become a valuable model organism for studies of the genetic interaction networks involving base excision repair (BER). As a first step towards characterization of BER in C. elegans, we show that the UNG-1 protein is an active uracil-DNA glycosylase. We demonstrate that an ung-1 mutant has reduced ability to repair uracil-containing DNA but that an alternative Ugi-inhibited activity is present in ung-1 nuclear extracts. Finally, we demonstrate that ung-1 mutants show altered levels of apoptotic cell corpses formed in response to DNA damaging agents. Increased apoptosis in the ung-1 mutant in response to ionizing radiation (IR) suggests that UNG-1 contributes to repair of IR-induced DNA base damage in vivo. Following treatment with paraquat however, the apoptotic corpse-formation was reduced. Gene expression profiling suggests that this phenotype is a consequence of compensatory transcriptomic shifts that modulate oxidative stress responses in the mutant and not an effect of reduced DNA damage signaling.
2010-05-26 | GSE21467 | GEO
Project description:The nematode Caenorhabditis elegans has been used extensively to study responses to DNA damage. In contrast, little is known about DNA repair in this organism. C. elegans is unusual in that it encodes few DNA glycosylases and the uracil-DNA glycosylase (UDG) encoded by the ung-1 gene is the only known UDG. C. elegans could therefore become a valuable model organism for studies of the genetic interaction networks involving base excision repair (BER). As a first step towards characterization of BER in C. elegans, we show that the UNG-1 protein is an active uracil-DNA glycosylase. We demonstrate that an ung-1 mutant has reduced ability to repair uracil-containing DNA but that an alternative Ugi-inhibited activity is present in ung-1 nuclear extracts. Finally, we demonstrate that ung-1 mutants show altered levels of apoptotic cell corpses formed in response to DNA damaging agents. Increased apoptosis in the ung-1 mutant in response to ionizing radiation (IR) suggests that UNG-1 contributes to repair of IR-induced DNA base damage in vivo. Following treatment with paraquat however, the apoptotic corpse-formation was reduced. Gene expression profiling suggests that this phenotype is a consequence of compensatory transcriptomic shifts that modulate oxidative stress responses in the mutant and not an effect of reduced DNA damage signaling. C. elegans RNAi mutants deficient in ung-1 and the corresponding wild-type N2, were subjected to Affymetrix whole C. elegans genome microarrays. Triplicates were run for each sample group.
2010-06-08 | E-GEOD-21467 | biostudies-arrayexpress
Project description:DNA base lesions, such as incorporation of uracil into DNA or base mismatches, can be mutagenic and toxic to replicating cells. To discover factors in repair of genomic uracil, we performed a CRISPR knockout screen in the presence of floxuridine, a chemotherapeutic agent that incorporates uracil and fluoro-uracil into DNA. We identified known factors, such as uracil DNA N-glycosylase (UNG), but also unknown factors, such as the N6-adenosine methyltransferase, METTL3, as required to overcome floxuridine-driven cytotoxicity. Visualized with immunofluorescence, the product of METTL3 activity, N6-methyladenosine, formed nuclear foci in cells treated with floxuridine. The observed N6-methyladenosine was embedded in DNA, called 6mA, which was confirmed using mass spectrometry. METTL3 and 6mA were required for repair of lesions driven by additional base damaging agents, including raltitrexed, gemcitabine, and hydroxyurea. Our results establish a role for METTL3 and 6mA to promote genome stability in mammalian cells, specially in response to base damage.
2024-11-22 | GSE282260 | GEO
Project description:To test the effects of uracil DNA glycosylase (UNG) loss on the formation of double strand breaks (DSBs) by the anti-cancer agent pemetrexed, we performed ChIP-seq for serine 139-phosphorylated H2AX (gammaH2AX), a marker of DSBs, in human cells wild-type or deficient for UNG in combination with pemetrexed treatment. UNG deficiency results in an increase in DSBs upon pemetrexed treatment, and we found that pemetrexed treatment induces DSBs at different genomic locations in UNG wild-type and knockout cells. Similar results were observed upon cisplatin treatment of UNG wild-type and knockout cells, and the genomic locations of DSBs were distinct between pemetrexed-treated and cisplatin-treated samples. Taken together, our results suggest differential mechanisms for DSB formation in UNG-competent and UNG-deficient cells.
2013-10-28 | GSE50692 | GEO
Project description:Homo sapiens ENSG00000254047, uracil-DNA glycosylase (UNG) pseudogene, is expressed in 2 baseline experiment(s);
| ENSG00000254047 | ExpressionAtlas
Project description:Homo sapiens ENSG00000248196, uracil-DNA glycosylase (UNG) pseudogene, is expressed in 24 baseline experiment(s);
| ENSG00000248196 | ExpressionAtlas
Project description:Homo sapiens ENSG00000261047, uracil-DNA glycosylase (UNG) pseudogene, is expressed in 6 baseline experiment(s);
| ENSG00000261047 | ExpressionAtlas
Project description:Homo sapiens ENSG00000254047, uracil-DNA glycosylase (UNG) pseudogene, is differentially expressed in 1 experiment(s);
| ENSG00000254047 | ExpressionAtlas
Project description:Homo sapiens ENSG00000248196, uracil-DNA glycosylase (UNG) pseudogene, is differentially expressed in 4 experiment(s);
| ENSG00000248196 | ExpressionAtlas
Project description:To test the effects of uracil DNA glycosylase (UNG) loss on the formation of double strand breaks (DSBs) by the anti-cancer agent pemetrexed, we performed ChIP-seq for serine 139-phosphorylated H2AX (gammaH2AX), a marker of DSBs, in human cells wild-type or deficient for UNG in combination with pemetrexed treatment. UNG deficiency results in an increase in DSBs upon pemetrexed treatment, and we found that pemetrexed treatment induces DSBs at different genomic locations in UNG wild-type and knockout cells. Similar results were observed upon cisplatin treatment of UNG wild-type and knockout cells, and the genomic locations of DSBs were distinct between pemetrexed-treated and cisplatin-treated samples. Taken together, our results suggst differential mechanisms for DSB formation in UNG-competent and UNG-deficient cells. The genomic distribution of gammaH2AX in UNG WT and KO cells treated with pemetrexed or cisplatin was determined by ChIP-seq
2013-10-28 | E-GEOD-50692 | biostudies-arrayexpress