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GEO help: Mouse over screen elements for information. |
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| 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
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| 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.
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| Overall design |
WGBS, RNA-seq, and ChIP-seq for histone H3 post-translational modifications in mouse embryonic stem cells (mESC).
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| 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 |
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| Submission date |
Oct 25, 2021 |
| Last update date |
Apr 11, 2022 |
| Contact name |
Carmen Rivas |
| E-mail(s) |
mcarmen.rivas@usc.es
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| Organization name |
Universidad de Santiago de Compostela
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| Department |
CIMUS
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| Lab |
P2L7
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| Street address |
Avda Barcelona
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| City |
Santiago de Compostela |
| ZIP/Postal code |
15706 |
| Country |
Spain |
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| Platforms (4)
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| GPL21103 |
Illumina HiSeq 4000 (Mus musculus) |
| GPL21273 |
HiSeq X Ten (Mus musculus) |
| GPL25475 |
Illumina HiSeq 4000 (Drosophila melanogaster; Mus musculus) |
| GPL29685 |
Illumina NovaSeq 6000 (Drosophila melanogaster; Mus musculus) |
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| Samples (28)
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| Relations |
| BioProject |
PRJNA774249 |
| SRA |
SRP342995 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE186506_RAW.tar |
15.4 Gb |
(http)(custom) |
TAR (of BIGWIG, BW, TDF) |
SRA Run Selector |
| Raw data are available in SRA |
| Processed data provided as supplementary file |
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