Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Regulation of 3D genome organization, transcription and histone H3K9me2 by histone H3K9 methyltransferases [RNA-Seq]

ABSTRACT: Histone H3 lysine 9 dimethylation (H3K9me2) is a highly conserved silencing epigenetic mark. Chromatin marked with H3K9me2 forms large domains in mammalian cells and overlaps well with lamina-associated domains and the B compartment defined by Hi-C. However, the role of H3K9me2 in 3-dimensional (3D) genome organization remains unclear. We investigated genome-wide H3K9me2 distribution, transcriptome, and 3D genome organization in mouse embryonic stem cells following the inhibition or depletion of five H3K9 methyltransferases (MTases): G9a, GLP, SETDB1, SUV39H1, and SUV39H2. H3K9me2 was regulated by all five MTases; however, H3K9me2 and transcription in the A and B compartments were regulated by different MTases. H3K9me2 in A compartments was primarily regulated by G9a/GLP and SETDB1, while H3K9me2 in the B compartments was regulated by all five MTases. Furthermore, decreased H3K9me2 correlated with changes to the more active compartmental state that accompanied transcriptional activation.

ORGANISM(S): Mus musculus

PROVIDER: GSE169098 | GEO | 2021/03/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Regulation of mammalian 3D genome organization and histone H3K9 dimethylation by H3K9 methyltransferases

Project description:Histone H3 lysine 9 dimethylation (H3K9me2) is a highly conserved silencing epigenetic mark. Chromatin marked with H3K9me2 forms large domains in mammalian cells and overlaps well with lamina-associated domains and the B compartment defined by Hi-C. However, the role of H3K9me2 in 3-dimensional (3D) genome organization remains unclear. We investigated genome-wide H3K9me2 distribution, transcriptome, and 3D genome organization in mouse embryonic stem cells following the inhibition or depletion of five H3K9 methyltransferases (MTases): G9a, GLP, SETDB1, SUV39H1, and SUV39H2. H3K9me2 was regulated by all five MTases; however, H3K9me2 and transcription in the A and B compartments were regulated by different MTases. H3K9me2 in A compartments was primarily regulated by G9a/GLP and SETDB1, while H3K9me2 in the B compartments was regulated by all five MTases. Furthermore, decreased H3K9me2 correlated with changes to the more active compartmental state that accompanied transcriptional activation.

2021-08-05 | PXD024756 | Pride

Regulation of 3D genome organization, transcription and histone H3K9me2 by histone H3K9 methyltransferases [HiC]

2021-03-18 | GSE169103 | GEO

Regulation of 3D genome organization, transcription and histone H3K9me2 by histone H3K9 methyltransferases [ChIP-Seq]

2021-03-18 | GSE169099 | GEO

Genome-wide maps of nuclear lamina interactions in AML12 cells upon G9a/GLP inhibition [DamID]

Project description:In differentiated cells, inhibition of methyltransferases G9a and GLP eliminated H3K9me2 predominantly at A-type genomic compartments, and the remaining H3K9me2 marks were strongly associated with B-type compartments and lamina-associated domains (LADs). However, inhibition of G9a/GLP in mouse embryonic stem cells (ESCs) removed most of the H3K9me2 modifications in both A and B compartments. Furthermore, chemical inhibition of G9a/GLP in mouse hepatocytes decreased chromatin-nuclear lamina (NL) interactions, increased the degree of genomic compartmentalization and the boundary strength of topologically associating domains (TADs) between A and B compartments, and altered the expression of hundreds of genes that were associated with alterations of chromatin structure.

2021-06-20 | GSE132957 | GEO

Identification of proteins stably associated with G9a/GLP (EHMT2/EHMT1) complex of histone methyltransferases

Project description:G9a (EHMT2) and the G9a-like protein GLP (EHMT1) form a stable G9a/GLP heterodimer in embryonic stem cells and function cooperatively to establish and maintain the abundant repressive H3K9me2 modification, in addition to modifying several non-histone proteins. The G9a-dependent H3K9me2 is implicated in lineage-specific gene silencing and covers large chromosomal domains. While the mechanism of H3K9me2maintenance by G9a/GLP is known, how new patterns of this modification are established is not well understood. With this in mind, we used FLAG affinity purification of G9a under two different stringency conditions (150 and 300 mM NaCl) coupled with mass spectrometry to identify proteins stably associated with G9a/GLP, which could serve as potential recruiters of the complex to unmodified chromatin.

2016-03-16 | PXD003466 | Pride

Spatial organization of H3K9me2/3-marked heterochromatin is redundantly maintained by either the H3K9 or H3K27 methylation pathway [MethylC-seq]

Project description:Heterochromatin is a key architectural feature of eukaryotic chromosomes, which is critical for cell type specific gene expression and genome stability. In the mammalian nucleus, heterochromatin is segregated from transcriptionally active genomic regions, and exists as large condensed and inactive nuclear compartment. However, the underlying mechanism of spatial organization of heterochromatin is still poorly understood. Histone H3 lysine 9 di- and tri-methylation (H3K9me2/3) and lysine 27 trimethylation (H3K27me3) are two major epigenetic modifications that define constitutive and facultative heterochromatin, respectively. In mammals, there are at least five H3K9 methyltransferases (SUV39H1, SUV39H2, SETDB1, G9a and GLP) and two H3K27 methyltransferases (EZH1 and EZH2). In this study, we addressed the role of H3K9 and H3K27 methylation in heterochromatin organization by using a combination of compound mutant cells for the five H3K9 methyltransferases and an EZH1/2 dual inhibitor, DS3201. We show that H3K27me3, which is normally segregated from H3K9me2/3, was redistributed to regions targeted by H3K9me2/3 after the loss of H3K9 methylation, and loss of both H3K9 and H3K27 methylation resulted in impaired both condensation and spatial organization of heterochromatin. Our data demonstrate that the two major repressive epigenome pathways exclusively but also coordinately maintain H3K9me2/3-marked heterochromatin organization in mammalian cells.

2022-04-05 | GSE200010 | GEO

Spatial organization of H3K9me2/3-marked heterochromatin is redundantly maintained by either the H3K9 or H3K27 methylation pathway [HistoneLamin]

2022-04-05 | GSE200014 | GEO

Spatial organization of H3K9me2/3-marked heterochromatin is redundantly maintained by either the H3K9 or H3K27 methylation pathway [Hi-C]

2022-04-05 | GSE200012 | GEO

Spatial organization of H3K9me2/3-marked heterochromatin is redundantly maintained by either the H3K9 or H3K27 methylation pathway [RNA-Seq]

2022-04-05 | GSE200015 | GEO

Spatial organization of H3K9me2/3-marked heterochromatin is redundantly maintained by either the H3K9 or H3K27 methylation pathway [ChIP-Seq]

2022-04-05 | GSE200011 | GEO