Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

NicE-seq in Suv39h2 knockdown 8-cell stage

ABSTRACT: Determination of accessible chromatin regions in the 8-cell stage mouse embryo after Suv39h2 knockdown The study aimed to address a potential function of H3K9me3 in early mouse development by assessing its impact on chromatin compaction. The histone methyltransferase responsible for de novo H3K9me3 at fertilization Suv39h2, was knocked down by microinjection of dsRNA targeting Suv39h2 in the early zygote. Embryos were then cultured until the 8-cell stage of development. They were then fixed and chromatin compaction was assessed by NicE-seq in pools of 10 8-cell stage embryos.

ORGANISM(S): Mus musculus

PROVIDER: GSE138686 | GEO | 2020/03/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

NicE-seq in Suv39h2 knockdown 8-cell stage

Project description:NicE-seq in Suv39h2 knockdown 8-cell stage

| PRJNA576800 | ENA

Loss of H3K9 tri-methylation alters chromosome compaction and transcription factor retention during mitosis

Project description:Recent studies have shown that repressive chromatin machinery, including DNA methyltransferases and Polycomb Repressor Complexes, bind to chromosomes throughout mitosis and their depletion results in increased chromosome size. Here we show that enzymes that catalyse H3K9 methylation, such as Suv39h1, Suv39h2, G9a and Glp, are also retained on mitotic chromosomes. Surprisingly however, mutants lacking H3K9me3 have unusually small and compact mitotic chromosomes associated with increased H3S10ph and H3K27me3 levels. Chromosome size and centromere compaction in these mutants were rescued by providing exogenous Suv39h1, or inhibiting Ezh2 activity. Quantitative proteomic comparisons of native mitotic chromosomes isolated from wildtype versus Suv39h1/Suv39h2 double-null mouse ESCs revealed that H3K9me3 was essential for the efficient retention of bookmarking factors such as Esrrb. These results highlight an unexpected role for repressive heterochromatin domains in preserving transcription factor binding through mitosis, and underscore the importance of H3K9me3 for sustaining chromosome architecture and epigenetic memory during cell division.

2023-01-25 | PXD039521 | Pride

Transcriptomic analysis in Suv39h2-deficient brain during early neurodevelopment

Project description:To examine the molecular phenotype of Suv39h2-deficits during early neurodevelopment, transcriptome analysis in the E11.5 brain of Suv39h2-deficient mouse and wild-type littermates were performed. The Suv39h2 mutation was made using CRISPR/Cas9n-mediated genome editing

2023-12-30 | E-MTAB-10528 | biostudies-arrayexpress

NicE-C efficiently reveals open chromatin associated chromosome interactions at high resolution

Project description:Enhancer-promoter communication is known to regulate spatiotemporal gene expression. Here, we present NicE-C, a method that leverages nicking enzyme mediated open chromatin profiling and chromosome conformation capture to enable robust and cost-effective detection of chromatin interactions among open chromatin regions (e.g., between enhancers and promoters). Demonstrating its application utility, NicE-C revealed dynamic enhancer-promoter interactions associated with gene expression changes after TNFɑ stimulation in HeLa cells and during aging process in mice kidney.

2022-01-18 | GSE176066 | GEO

Loss of H3K9 tri-methylation alters mitotic chromosome compaction and transcription factor retention during mitosis

Project description:Recent studies have shown that repressive chromatin machinery, including DNA methyltransferases (DNMTs) and Polycomb Repressor Complexes (PRCs), bind to chromosomes throughout mitosis and their depletion results in increased chromosome size. Enzymes that catalyse H3K9 methylation, such as Suv39h1, Suv39h2, G9a, GLP are also retained by mitotic chromosomes. Surprisingly however, mutants lacking H3K9me3 have unusually small and compact mitotic chromosomes that are associated with increased H3S10ph and H3K27me3 levels. Chromosome size and centromere compaction in these mutants was rescued by providing exogenous Suv39h1, or inhibiting Ezh2 activity. Quantitative proteomic comparisons of native mitotic chromosomes isolated from wildtype versus Suv39h1,2 double null ESCs revealed that H3K9me3 was essential for the efficient retention of bookmarking factors such as Esrrb. These results highlight an unexpected role for repressive heterochromatin domains in preserving transcription factor binding through mitosis, and underscore the importance of H3K9me3 for sustaining chromosome architecture and epigenetic memory during cell division.

2022-10-12 | PXD030771 | Pride

NicE-seq: high resolution open chromatin profiling

Project description:Mammalian chromatin is dynamic and contains structural information that leads to transcriptional regulation of genes by recruiting transcription factors and altering nucleosome positioning. Here, we describe open chromatin mapping using Nicking Enzyme assisted sequencing (NicE-seq) for integrative epigenomic analysis. NicE-seq captures open chromatin sites in both fixed and native cells and reveals the genomic location of open chromatin sites (OCS) and transcription factor occupancy at single nucleotide resolution, with as few as 250 HCT116 cells. In HCT116 cells a large percentage of the OCS were coincident with DHS (DNaseI hypersensitive site) and ATAC-seq sites. OCSs correlated well with RNA pol II occupancy and transcriptionally active chromatin marks, while displaying a pattern contrasting to CpG methylation. ChIP CTCF peaks common to OCS and DHS displayed a strong correlation with H3K4me3 and H3K27ac marks. Further peaks unique to OCS and ChIP CTCF peaks also correlated strongly with H3K4me3, H3K27ac and higher transcription. Similar results were also obtained for Max and Sp1 transcription factors. Using NicE-seq we have demonstrated that HCT116 cells, treated with anti cancer drug decitabine, displayed time dependent accumulation of OCS coinciding with hypomethylation of the genome, particularly in SINE and satellite repetitive DNA. Differentially methylated regions (DMRs) were more pronounced in promoters, 5’UTR, CpG islands and exons. In summary, sequence specificity offered by a nicking enzyme allows a means to study open chromatin structure and hypomethylation of genomes, revealing the open chromatin landscape in cellular context.

2017-05-24 | GSE97889 | GEO

RNA-seq profiles of DP thymocytes from control and Suv39h1/Suv39h2 double knockout mice

2024-03-27 | GSE156296 | GEO

SUV39H2 CONTROLS TROPHOBLAST STEM CELL FATE

Project description:The placenta is constructed through the orchestration of trophoblast stem (TS) cell expansion and differentiation along a multi-lineage pathway. Dynamic regulation of histone H3K9 methylation is pivotal to cell differentiation for many cell lineages, but little is known about its involvement in trophoblast development. Among the twelve-known histone H3K9 methyltransferases, only SUV39H2 exhibited robust differential expression in stem versus differentiated rat TS cells. SUV39H2 transcript and protein expression were high in the stem state and rapidly declined as TS cells differentiated. Disruption of SUV39H2 expression in TS cells led to prominent phenotypic changes. Suv39h2-specific shRNA knockdown resulted in an arrest in TS cell proliferation and activation of trophoblast cell differentiation. These observations were reinforced by flow cytometry and transcript profiling. Histone H3K9 methylation status at specific loci exhibiting differentiation-dependent gene expression were regulated by SUV39H2 and also represented sites for SUV39H2 occupancy. Analyses of SUV39H2 on ex vivo rat blastocyst development supported its role in regulating TS cell expansion and differentiation. Finally, we identified SUV39H2 as a downstream target of CDX2, a master regulator of trophoblast lineage development. In summary, our findings indicate that SUV39H2 contributes to the maintenance of the TS cell stem state and restrains trophoblast cell differentiation and thus serves as a contributor to the epigenetic regulation of hemochorial placental development.

2021-07-15 | GSE154701 | GEO

in situ Hi-C profiles of DP thymocyltes from control and Suv39h1/Suv39h2 double knockout mice

Project description:H3K9me3-dependent heterochromatin is critical for the silencing of repeat-rich pericentromeric regions and also has key roles in repressing lineage-inappropriate protein-coding genes for healthy cellular function. Here we investigate the disruption of genome organization in the absence of H3K9me3-dependent heterochromatin by performing in situ Hi-C in primary immune cells deficient in both Suv39h1 and Suv39h2 (Suv39DKO), the major mammalian histone methyltransferase enzymes which catalyse heterochromatic H3K9me3 deposition.

2024-03-27 | GSE156294 | GEO

ATAC-seq of DP thymocytes from Suv39h1 and Suv39h2 double knockout chimeric mice

Project description:H3K9me3-dependent heterochromatin is critical for the silencing of repeat-rich pericentromeric regions and also has key roles in repressing lineage-inappropriate protein-coding genes for healthy cellular function. Within all eukaryotic nuclei, heterochromatin and euchromatin are spatially segregated, with euchromatin typically located in the nuclear interior and heterochromatin at the nuclear periphery. Here we investigate the changes in DNA accessibilty in the absence of H3K9me3-dependent heterochromatin by performing ATAC-seq in primary immune cells deficient in both Suv39h1 and Suv39h2 (Suv39DKO), the major mammalian histone methyltransferase enzymes which catalyse heterochromatic H3K9me3 deposition.

2024-03-27 | GSE256244 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data