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Series GSE186506 Query DataSets for GSE186506
Status Public on Mar 28, 2022
Title H3K36 Dimethylation Shapes the Epigenetic Interaction Landscape by Directing Repressive Chromatin Modifications in Embryonic Stem Cells
Organisms Drosophila melanogaster; Mus musculus
Experiment type Expression profiling by high throughput sequencing
Genome binding/occupancy profiling by high throughput sequencing
Methylation profiling by high throughput sequencing
Summary Epigenetic modifications on the chromatin do not occur in isolation. Chromatin associated proteins and their modification products form a highly interconnected network, and disturbing one component may rearrange the entire system. We see this increasingly clearly in epigenetically dysregulated cancers. It is important to understand the rules governing epigenetic interactions. Here, we use the mouse embryonic stem cell (mESC) model to describe in detail the relationships within the H3K27-H3K36-DNA methylation subnetwork. In particular, we focus on the major epigenetic re-organization caused by deletion of the histone 3 lysine 36 methyltransferase NSD1, which in mESCs deposits nearly all of the intergenic H3K36me2. Although disturbing the H3K27 and DNA methylation (DNAme) components also affects this network to a certain extent, the removal of H3K36me2 has the most drastic effect on the epigenetic landscape, resulting in full intergenic spread of H3K27me3 and a substantial decrease in DNAme. By profiling DNMT3A and CHH methylation (mCHH), we show that H3K36me2 loss upon Nsd1-KO leads to a massive re-distribution of DNMT3A and mCHH away from intergenic regions and towards active gene bodies, suggesting that DNAme reduction is at least in part caused by redistribution of de novo methylation. Additionally, we show that pervasive acetylation of H3K27 is regulated by the interplay of H3K36 and H3K27 methylation. Our analysis highlights the importance of H3K36me2 as a major determinant of the developmental epigenome and provides a framework for further consolidating our knowledge of epigenetic networks.
 
Overall design WGBS, RNA-seq, and ChIP-seq for histone H3 post-translational modifications in mouse embryonic stem cells (mESC).
 
Contributor(s) Chen H, Hu B, Horth C, Bareke E, Rosenbaum P, Kwon SY, Sirois J, Weinberg DN, Lu C, Pastor WA, Majewski J
Citation(s) 35396277
Submission date Oct 25, 2021
Last update date Apr 11, 2022
Contact name Carmen Rivas
E-mail(s) mcarmen.rivas@usc.es
Organization name Universidad de Santiago de Compostela
Department CIMUS
Lab P2L7
Street address Avda Barcelona
City Santiago de Compostela
ZIP/Postal code 15706
Country Spain
 
Platforms (4)
GPL21103 Illumina HiSeq 4000 (Mus musculus)
GPL21273 HiSeq X Ten (Mus musculus)
GPL25475 Illumina HiSeq 4000 (Drosophila melanogaster; Mus musculus)
Samples (28)
GSM5653814 H3K27me3_ChIP-seq_mESC_Parental
GSM5653815 H3K27me2_ChIP-seq_mESC_Parental
GSM5653816 H3K27me1_ChIP-seq_mESC_Parental
Relations
BioProject PRJNA774249
SRA SRP342995

Download family Format
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Supplementary file Size Download File type/resource
GSE186506_RAW.tar 15.4 Gb (http)(custom) TAR (of BIGWIG, BW, TDF)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data provided as supplementary file

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