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H3K36me3 ChIP-seq in non-treated and raltitrexed-treated UGI-expressing HCT116 cells

ABSTRACT: We report ChIP-seq for H3K36me3 that were performed as supplementary experiments to the U-DNA-Seq study (GSE126822). H3K36me3 ChIP-seq was conducted in raltitrexed (RTX) treated or non-treated (NT) HCT116 cells expressing the UNG inhibitor (UGI). We found that the applied RTX treatment did not result in major differences in the genome-wide distribution of the H3K36me3 histone marker. For wider context of the study, see the related publication.

ORGANISM(S): Homo sapiens

PROVIDER: GSE153407 | GEO | 2020/09/20

REPOSITORIES: GEO

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Genome-wide alterations of uracil distribution patterns in human DNA upon chemotherapeutic treatments

Project description:We report a new immunoprecipitation-coupled sequencing (DIP-Seq) application termed U-DNA-Seq, where a tailored and catalytically inactive uracil-DNA glycosylase (UNG) was used as uracil-DNA sensor to immunoprecipitate uracil containing genomic DNA fragments. Genomic uracil was profiled in drug-treated (5-fluoro-2'-deoxyuridine (5FdUR) or raltitrexed (RTX)) or non-treated (NT) HCT116 cells expressing the UNG inhibitor (UGI). The same experiments were also performed in the mismatch repair proficient version of the HCT116 cells (HCT116MMR), where chromosome 3 is reinserted to restore functional MMR (PMID: 8044777). Moreover, wild-type HCT116 or K562 cells were also measured. We found that regions of uracil enrichment in this assay were rather broad as compared to the sharp peaks typical in ChIP-seq. Therefore, we applied an approach alternative to the conventional peak calling. Namely, we calculated genome scaled coverage tracks and log2 ratio tracks of the enriched versus the input samples using deepTools package (bamCoverage and bigwigCompare tools, respectively) to provide a more appropriate description of uracil-enriched genomic regions. Interval (bed) files were also derived from these log2 ratio tracks to be able to screen large datasets for colocalizing features with them. For wider context of the study, see the related publication.

2020-09-20 | GSE126822 | GEO

H3K36me3 ChIP-seq in non-treated and raltitrexed-treated UGI-expressing HCT116 cells

Project description:H3K36me3 ChIP-seq in non-treated and raltitrexed-treated UGI-expressing HCT116 cells

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Loss of Caenorhabditis elegans UNG-1 uracil-DNA glycosylase affects apoptosis in response to DNA damaging agents.

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

Targeted Profiling of Epitranscriptomic Reader, Writer and Eraser Proteins Regulated by H3K36me3

Project description:Trimethylation of lysine 36 on histone H3 (H3K36me3), an epigenetic mark associated with actively transcribed genes, plays an important role in multiple cellular processes, including transcription elongation, DNA methylation, DNA repair, and RNA m6A methylation, etc. Aberrant expression and mutations of the main methyltransferase for H3K36me3, i.e., SET domain-containing 2 (SETD2), were shown to be associated with various cancers. Here, we performed targeted profiling of 154 epitranscriptomic RWE proteins using a scheduled liquid chromatography-parallel-reaction monitoring (LC-PRM) method coupled with the use of stable isotope-labeled (SIL) peptides as internal standards to investigate how H3K36me3 modulates the chromatin occupancies of epitranscriptomic reader, writer, and eraser (RWE) proteins. Our results showed consistent changes in chromatin occupancies of RWE proteins upon losses of H3K36me3 and H4K16ac, and a role of H3K36me3 in recruiting METTL3 to chromatin upon DNA double strand break induction. In addition, protein-protein interaction network and Kaplan-Meier survival analyses revealed the importance of METTL14 and TRMT11 in kidney cancer. Taken together, our work revealed cross-talks between H3K36me3 and epitranscriptomic RWE proteins and uncovered potential roles of these RWE proteins in H3K36me3-mediated biological processes.

2023-05-25 | PXD041343 | Pride

Loss of Caenorhabditis elegans UNG-1 uracil-DNA glycosylase affects apoptosis in response to DNA damaging agents.

2010-06-08 | E-GEOD-21467 | biostudies-arrayexpress

UNG shapes the specifity of AID-induced somatic hypermutation in non B cells

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2012-07-04 | E-GEOD-39108 | biostudies-arrayexpress

H3K36me3 profiling in mTEClo

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ChIPSeq of H3k36me3 samples of OSKM reprogramming mouse embryonic fibroblasts treated with B12

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2023-08-07 | GSE200578 | GEO

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Project description:These are the RNAseq data in the publication. The detailed information can be obtained from the supplementary tables in the paper.

2021-03-14 | GSE157517 | GEO

ChIP-Seq sequencing of novel interactors of H3K4me3, H3K36me3 and H3K9me3

Project description:This study describes the epigenetic profiling of the novel interactors of H3K4me3, H3K36me3 or H3K9me3. The interactors were ChIP-Seq profiled by their GFP tag in stably transfected HeLa (Kyoto) cells. The interactors include GATAD1, Sgf29, BAP18, TRRAP, PHF8, N-PAC and LRWD1 (including replicates), as well as an GFP ChIP-Seq profile on non-transfected HeLa cells (negative control). Also included are the profiles of the histone modifications themselves (H3K4me3, H3K27me3, H3K9me3, H3K36me3, H3K9/14Ac and H3K79me3) ChIP-Seq profiling of 8 proteins by their GFP tag in stably transfected cells HeLa (Kyoto) cells, 6 replicas, as well as ChIP-Seq profiling of 6 histone modifications in wt HeLa (Kyoto) cells

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