Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

SETDB1/NSD dependent H3K9me3/H3K36me3 dual heterochromatin maintains gene expression profiles by bookmarking poised enhancers

ABSTRACT: Gene silencing by heterochromatin plays crucial roles in cell identity and development. However, the function of heterochromatin components is not fully understood. Here, we characterize the localization, the biogenesis and the function of an atypical heterochromatin, which is simultaneously enriched in the typical heterochromatin mark H3K9me3 as well as in H3K36me3, histone mark usually associated with gene expression. This dual heterochromatin forms on 3,015 regions in the genome of mouse embryonic stem cells and relies on the histone methyltransferases SET Domain Bifurcated 1 (SETDB1) and Nuclear Set Domain containing proteins (NSD) to generate H3K9me3 and H3K36me3, respectively. Upon SETDB1 removal, dual domains loose both trimethyl marks, gain epigenomic signatures of active enhancers, and come into long range contact with upregulated genes, suggesting that it is a major pathway by which gene expression is controlled by heterochromatin. In differentiated tissues, a large subset of these dual domains is destabilized and become enriched in active enhancer marks, providing a mechanistic insight into the involvement of heterochromatin in development and the maintenance of cell identity.

ORGANISM(S): Mus musculus

PROVIDER: GSE171749 | GEO | 2022/01/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

SETDB1/NSD dependent H3K9me3/H3K36me3 dual heterochromatin maintains gene expression profiles by bookmarking poised enhancers

Project description:SETDB1/NSD dependent H3K9me3/H3K36me3 dual heterochromatin maintains gene expression profiles by bookmarking poised enhancers

| PRJNA720715 | ENA

proj022_chipseq

Project description:The mechanisms that recruit the major Polycomb-group (PcG) complexes PRC1 and PRC2 to target sites in vertebrate cells are not well understood. Building on recent studies that have determined a reciprocal relationship between DNA methylation and Polycomb activity, we demonstrate that in methylation deficient ES cells CpG density, combined with antagonistic effects of H3K9me3 and H3K36me3, redirect PcG complexes to pericentric heterochromatin and gene rich domains. In this experiment we have assayed the genomic distribution of H3K9me3 and H3K36me3 marks,

2014-05-23 | E-MTAB-2481 | biostudies-arrayexpress

Mechanism suppressing H3K9 trimethylation in pluripotent stem cells and its demise by polyQ-expanded huntingtin mutations [ChIP-seq]

Project description:We find that HTT binds ATF7IP, a regulator of the histone H3 methyltransferase SETDB1. HTT inhibits the interaction of the ATF7IP-SETDB1 complex with other heterochromatin regulators and transcriptional repressors, maintaining low levels of H3K9 trimethylation (H3K9me3) in hESCs. Conversely, loss of HTT promotes global increased H3K9me3 levels. To test whether HTT knockdown also induces enrichment of H3K9me3 marks at specific genes, we performed chromatin immunoprecipitation (ChIP)-sequencing assays of hESCs using an antibody to H3K9me3.

2018-09-04 | GSE118324 | GEO

Mechanism suppressing H3K9 trimethylation in pluripotent stem cells and its demise by polyQ-expanded huntingtin mutations [RNA-seq]

2018-09-04 | GSE118088 | GEO

A feedback loop between heterochromatin and the nucleopore complex controls germ-cell to oocyte transition during Drosophila oogenesis [Cut&Run]

Project description:Germ cells differentiate into oocytes that become totipotent upon fertilization. How the highly specialized oocyte acquires this distinct cell fate is poorly understood. During Drosophila oogenesis, H3K9me3 histone methyltransferase SETDB1 translocates from the cytoplasm to the nucleus of germ cells concurrent with oocyte specification. Here, we discovered that nuclear SETDB1 is required to silence a cohort of differentiation-promoting genes by mediating their heterochromatinization. Intriguingly, SETDB1 is also required for the upregulation of 18 of the ~30 nucleoporins (Nups) that comprise the nucleopore complex (NPC). NPCs in turn anchor SETDB1-dependent heterochromatin at the nuclear periphery to maintain H3K9me3 and gene silencing in the egg chambers. Aberrant gene expression due to loss of SETDB1 or Nups results in loss of oocyte identity, cell death and sterility. Thus, a feedback loop between heterochromatin and NPCs promotes transcriptional reprogramming at the onset of oocyte specification that is critical to establish oocyte identity.

2023-08-08 | GSE186974 | GEO

A feedback loop between heterochromatin and the nucleopore complex controls germ-cell to oocyte transition during Drosophila oogenesis [mRNA-Seq]

2023-08-08 | GSE186970 | GEO

Reader interactome of epigenetic histone marks in birds

Project description:Lysine methylation is part of the posttranscriptional histone code employed to recruit modification specific readers to chromatin. Unbiased, quantitative mass spectrometry approaches combined with peptide pull-downs have been used to study histone methylation-dependent binders in mammalian cells. Here, we extend the study to birds by investigating the interaction partners for H3K4me3, H3K9me3, H3K27me3 and H3K36me3 in chicken (gallus gallus) and zebra finch (taeniopygia guttata) using label free quantitative proteomics. In general, we find very strong overlap in interaction partners for the trimethyl marks in birds compared to mammals, underscoring the known conserved function of these modifications. In agreement with their epigenetic role, we find binding of PHF2 and members of the TFIID, SAGA, SET1 and NURF complex to the activation mark H3K4me3. Our data furthermore supports the existence of a LID complex in vertebrates recruited to the H3K4me3. The repressive marks are bound by the HP1 proteins and the EED subunit of the PRC2 complex as well as by WIZ. Like the screens in mammals, we found ZNF462, ZNF828 and POGZ enriched at H3K9me3. However, we noted some unexpected differences. First, we did not observe the enrichment of CDYL and CDYL2 at the repressive marks. Second N-PAC (also known as GLYR1), an H3K36me3 interactor in mammals, is not binding to this modification in our screen. This suggests that despite strong conservation of the histone tail sequence, species-specific differences in epigenetic readers may have evolved.

2016-01-04 | PXD002282 | Pride

Crosstalk between gene body DNA methylation, H3K9me3 and H3K36me3 chromatin marks and transcription

Project description:This SuperSeries is composed of the following subset Series: GSE26018: Crosstalk between gene body DNA methylation, H3K9me3 and H3K36me3 chromatin marks and transcription [HuEx-1_0-st] GSE26019: Crosstalk between gene body DNA methylation, H3K9me3 and H3K36me3 chromatin marks and transcription [HuGene-1_0-st] GSE26038: Crosstalk between gene body DNA methylation, H3K9me3 and H3K36me3 chromatin marks and transcription [HuEx-1_0-st, transcript] GSE26040: Relationship between gene body DNA methylation and intragenic H3K9me3 and H3K36me3 chromatin marks Refer to individual Series

2011-03-31 | E-GEOD-26020 | biostudies-arrayexpress

Application of Histone Interacting Domains as an Alternative to Antibodies (CIDOP-seq)

Project description:Application of Histone Modification Interacting Domains (HMIDs) as an Alternative to Antibodies. HMIDs and antibodies (taken from ENCODE) were used for precipitation of native chromatin (mononucleosomes) in order to study distinct histone marks. HMIDs used in this study are MPP8 Chromo domains and ATRX ADD (as H3K9me3 binders), Dnmt3a PWWP (as H3K36me3 binder) and CBX7 Chromo (as H3K27me3 binder).

2014-02-06 | E-MTAB-2143 | biostudies-arrayexpress

Setdb1 is required for persistence of H3K9me3 and repression of endogenous retroviruses in mouse primordial germ cells

Project description:Transcription of endogenous retroviruses (ERVs) is inhibited by de novo DNA methylation during gametogenesis, a process initiated after birth in oocytes and at ~E15.5 in prospermatogonia. Earlier in germline development however, the genome, including most retrotransposons, is progressively demethylated, with young ERVK and ERV1 elements retaining intermediate methylation levels. As DNA methylation reaches a low point in E13.5 primordial germ cells (PGCs) of both sexes, we determined whether retrotransposons are marked by H3K9me3 and H3K27me3 using a recently developed low input ChIP-seq method. Although these repressive histone modifications are predominantly found on distinct genomic regions in E13.5 PGCs, they concurrently mark partially methylated LTRs and LINE1 elements. Germline-specific conditional knock-out (KO) of the H3K9 methyltransferase SETDB1 yields a decrease of both histone marks and DNA methylation at H3K9me3 enriched retrotransposon families. Strikingly, Setdb1-KO E13.5 PGCs show concomitant de-repression of many marked ERVs, including IAP, ETn and ERVK10C elements and ERV-proximal genes, a subset in a sex-dependent manner. Furthermore, Setdb1 deficiency is associated with a reduced number of male PGCs and postnatal hypogonadism in both sexes. Taken together, these observations reveal that SETDB1 is an essential guardian against proviral expression prior to the onset of de novo DNA methylation in the germline. H3K9me3, H3K27me3 and expression profiles in Setdb1 WT, Het and KO male and female E13.5 PGCs.

2014-09-01 | E-GEOD-60377 | biostudies-arrayexpress

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