Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dynamic enhancer partitioning instructs Zdbf2 activation during epigenetic reprogramming [RNA-Seq]

ABSTRACT: Early mammalian development is accompanied by a profound global remodeling of chromatin-based regulation. The Zdbf2 locus provides a valuable model to uncover the effect of dynamic chromatin transition, as it is polycomb silenced in embryonic stem cells (ESCs) and only becomes activated after Long isoform of Zdbf2 (Liz) transcription-dependent de novo DNA methylation during differentiation. Here we show that four enhancers contribute to the Liz-to-Zdbf2 promoter switch, concomitantly with dynamic changes in chromatin architecture. CTCF plays a key role in partitioning the locus in ESCs, when Liz is active and Zdbf2 is silenced. The partition is relieved when Zdbf2 becomes DNA methylated and active. Mutant ESCs that lack the partition fail to properly activate Zdbf2. Notably, the CTCF-based regulation occurs independently of the polycomb and DNA methylation pathways, suggesting a multi-layered regulatory framework that ensures proper epigenetic programming of a developmentally important gene.

ORGANISM(S): Mus musculus

PROVIDER: GSE121403 | GEO | 2019/04/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Dynamic enhancer partitioning instructs Zdbf2 activation during epigenetic reprogramming [bisulfite-seq]

Project description:Early mammalian development is accompanied by a profound global remodeling of chromatin-based regulation. The Zdbf2 locus provides a valuable model to uncover the effect of dynamic chromatin transition, as it is polycomb silenced in embryonic stem cells (ESCs) and only becomes activated after Long isoform of Zdbf2 (Liz) transcription-dependent de novo DNA methylation during differentiation. Here we show that four enhancers contribute to the Liz-to-Zdbf2 promoter switch, concomitantly with dynamic changes in chromatin architecture. CTCF plays a key role in partitioning the locus in ESCs, when Liz is active and Zdbf2 is silenced. The partition is relieved when Zdbf2 becomes DNA methylated and active. Mutant ESCs that lack the partition fail to properly activate Zdbf2. Notably, the CTCF-based regulation occurs independently of the polycomb and DNA methylation pathways, suggesting a multi-layered regulatory framework that ensures proper epigenetic programming of a developmentally important gene.

2019-04-18 | GSE121402 | GEO

Dynamic enhancer partitioning instructs Zdbf2 activation during epigenetic reprogramming [ATAC-Seq]

2019-04-18 | GSE121400 | GEO

Dynamic enhancer partitioning instructs Zdbf2 activation during epigenetic reprogramming [4C-Seq]

2019-04-18 | GSE121399 | GEO

Liz transcription is required for evicting H3K27me3 marks at the Gpr1/Zdbf2 locus through the deposition of DNA methylation marks.

Project description:To study the role of the Liz transcript on local chromatin features during early development, we used a culture-based system. Mouse embryonic stem cells (ESCs) with a hypomethylated genome were obtained through their culture in 2i medium supplemented with vitamin C. To recapitulate de novo DNA methylation, these cells were directed towards an epiblast-like cell fate (EpiLC) during seven days of culture in Activin A and Fgf2. The effect of Liz transcription on the maintenance of H3K27me3 marks at the Gpr1/Zdbf2 locus was inferred by the comparative ChIP-seq analysis of H3K27me3 enrichment in WT (E14) cells versus ∆Liz cells- which carry a TALEN-engineered 1.7kb homozygous deletion of the Liz Transcription Start Size (TSS)- at Day 0 (D0), D4 and D7 of EpiLC differentiation.

2016-11-01 | GSE79549 | GEO

Chip-chip from WT and Polycomb Component Kock Out Mouse ES cells for H2AZ, H3K27me3, EZH2 and Ring1B.

Project description:The essential histone variant H2A.Z localises to both active and silent chromatin sites. In embryonic stem cells (ESCs), H2A.Z is also reported to co-localise with polycomb repressive complex 2 (PRC2) at developmentally silenced genes. The mechanism of H2A.Z targeting is not clear, but a role for the PRC2 component Suz12 has been suggested. Given this association, we wished to determine if polycomb functionally directs H2A.Z incorporation in ESCs. We demonstrate that the PRC1 component Ring1B interacts with multiple complexes in ESCs. Moreover, we show that although the genomic distribution of H2A.Z co-localises with PRC2, Ring1B and with the presence of CpG islands, H2A.Z still blankets polycomb target loci in the absence of Suz12, Eed (PRC2) or Ring1B (PRC1). Therefore we conclude that H2A.Z accumulates at developmentally silenced genes in ESCs in a polycomb independent manner. Array design includes 2 biological replicates for all samples and technical replication (dye swaps for H3K27me3_WT_ES, EZH2_WT_ES, EZH2_RING1b_KO_ES, H2AZ_WT_ES(2), H2AZ_Eed_KO_ES and H2AZ_Suz12_KO_ES). Ring1B_WT_ES is represented by a single replicate.

2012-04-15 | E-GEOD-36999 | biostudies-arrayexpress

The imprinted Zdbf2 gene finely tunes hypothalamic control of feeding and growth in neonates.

Project description:To allow identification of differentially expressed genes between WT and Zdbf2-KO hypothalamus in mouse pups at 3 and 10dpp, mutants and control RNA-seq were conducted starting from whole hypothalamus RNA.

2022-01-24 | GSE153265 | GEO

Chip-chip from WT and Polycomb Component Knock Out Mouse ES cells for H2AZ, H3K27me3, EZH2 and Ring1B.

2012-04-16 | GSE36999 | GEO

The impact of the embryonic DNA methylation program on CTCF-mediated genome regulation

Project description:During mammalian embryogenesis, both the 5-cytosine DNA methylation (5meC) landscape and three dimensional (3D) chromatin architecture are profoundly remodeled during a process known as 'epigenetic reprogramming.' An understudied aspect of epigenetic reprogramming is how the 5meC flux, per se, affects the 3D genome. This is pertinent given the 5meC-sensitivity of DNA binding for a key regulator of chromosome folding: CTCF. We profiled the CTCF binding landscape using a mouse embryonic stem cell (ESC) differentiation protocol that models embryonic 5meC dynamics. Mouse ESCs lacking DNA methylation machinery are able to exit naive pluripotency, thus allowing for dissection of subtle effects of CTCF on gene expression. We performed CTCF HiChIP in both wild-type and mutant conditions to assess gained CTCF-CTCF contacts in the absence of 5meC. We performed H3K27ac HiChIP to determine the impact that ectopic CTCF binding has on cis-regulatory contacts. Using 5meC epigenome editing, we demonstrated that the methyl-mark is able to impair CTCF binding at select loci. Finally, a detailed dissection of the imprinted Zdbf2 locus showed how 5meC-antagonism of CTCF allows for proper gene regulation during differentiation. This work provides a comprehensive overview of how 5meC impacts the 3D genome in a relevant model for early embryonic events.

2024-07-23 | GSE246984 | GEO

Targeted DNA methylation analysis of the imprinted loci FAM50B and ZDBF2 in a cohort of small for gestational age born children

Project description:In this cohort of 52 individuals born small for gestational age we analyzed the DNA methylation of the two imprinted genes ZDBF2 and FAM50B using CpGs from these loci represented on the Illumina Infinium HumanMethylation450k Bead Chip.This cohort partly overlaps with an already published cohort analyzed for the potential influence of growth hormone therapy on the DNA methylation (GSE57205). Our analysis revealed one individual with a hypermethylation in ZDBF2.

2016-12-31 | GSE78035 | GEO

CTCF binding in B cells and Plasmablasts

Project description:The mammalian CCCTC-binding factor (CTCF) regulates gene expression through the formation of higher order chromatin structures. Recent evidence has implicated a role for CTCF in regulating gene expression in the human MHCII locus. To investigate the role of CTCF in murine MHCII gene expression we mapped CTCF binding sites in B cells (MHCII+ cells) and Plasmablasts which are differentiated B cells that have silenced MHCII gene expression. These observations lead to the identification of differential CTCF binding during differentiation in these cell types and suggest mechanims of MHCII gene regulation. Comparison of CTCF binding in B cells and Plasmablasts in mice using ChIP-seq

2014-02-05 | E-GEOD-44637 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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