ATAC-seq of wildtype or Dppa2 knockout ESC upon release of the epigenetic editing trigger
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ABSTRACT:
PROVIDER: PRJEB45210 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR5954183_1.fastq.gz | Fastqsanger.gz | |||
| ERR5954183_2.fastq.gz | Fastqsanger.gz | |||
| ERR5954184_1.fastq.gz | Fastqsanger.gz | |||
| ERR5954184_2.fastq.gz | Fastqsanger.gz | |||
| ERR5954185_1.fastq.gz | Fastqsanger.gz |
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Project description:Chromatin accessibility was assayed in wildtype or Dppa2 knockout ESC after 26 days of release of the trigger imposed by epigenetic editing. Samples were collected in two clonal knockout and wildtype lines after sorting at FACS of cells which maintained a repressive Esg1-tdTomato (TOMneg) reporter expression after 26 days of DOX washout (release of the trigger).
2021-11-23 | E-MTAB-10522 | biostudies-arrayexpress
Project description:Chromatin accessibility was assayed in ESC after epigenetic editing with dCas9::KRAB (or dCas9::GFP as a control) and subsequently in ESC and Endoderm differentiated cells upon release of the trigger. Samples were collected in two biological replicates after 7 days of DOX induction in ESC (epigenetic editing) and after 7 days of DOX washout (release of the trigger) in ESC and Endoderm cells.
2021-11-23 | E-MTAB-10523 | biostudies-arrayexpress
Project description:Enrichment of histone marks was assessed by CUT&RUN-sequencing after epigenetic editing with dCas9::KRAB (or dCas9::GFP as a control) and subsequently upon release of the trigger. Samples were collected after 7 days of DOX induction (epigenetic editing) and after 4 and 7 days of DOX washout (release of the trigger).
2021-11-23 | E-MTAB-10525 | biostudies-arrayexpress
Project description:ATAC-seq of ESC or in vitro differentiated endoderm cells after epigenetic editing and upon release of the trigger
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Project description:To understand the role of DPPA2 in epigenetic memory during X-Chromosome reactivation (XCR) we employed inducible Xist hybrid female embryonic stem cell line (TX1072, hybrid Bl6/Cast). Wild type or Dppa2 knockout TX1072 cells were cultured, in three or two independent biological replicates, respectively, in presence of DOX (1ug/ml) for 6 days to induce Xist overexpression and X-Chomosome inactivation (XCI) on the Bl6 allele. DOX was then washed out to silence Xist and XCR was followed in a time-series at 1, 3 or 7 days after DOX removal. Cell pellets were harvested at the following timepoints: -DOX, +DOX, 1d D-wo, 3d D-wo and 7d D-wo. RNA was extracted and 250 ng used for PolyA mRNA library preparation and Next generation sequencing.
2021-11-23 | E-MTAB-11183 | biostudies-arrayexpress
Project description:RNAseq in Dppa2 knockout or wildtype TX1072 ESC during and after Xist over-expression
| PRJEB48826 | ENA
Project description:Epigenetic priming factors establish a permissive epigenetic landscape which is not required until a later developmental or physiological time point, temporally uncoupling the presence of these factors with their phenotypic effects. One classic example of epigenetic priming is in the context of bivalent chromatin, found in pluripotent stem cells and early embryos at key developmental gene promoters marked by both activating-associated H3K4me3 and repressive-associated H3K27me3 histone modifications. It is currently unknown how these bivalent domains are targeted, or precisely how they impact on lineage commitment. Here we show that the small heterodimerising non-enzymatic DNA binding proteins Developmental Pluripotency Associated 2 (Dppa2) and 4 (Dppa4) act as epigenetic priming factors to establish bivalency at a subset of developmental genes. Dppa2/4 localise to the +1 nucleosome position of bivalent genes and while they are not required for pluripotency in embryonic stem cells (ESCs), double knockout cells fail to exit pluripotency and to differentiate efficiently, with delays in upregulating bivalently marked lineage genes. Proteomics reveal that Dppa2/4 interact on chromatin with members of the COMPASS and Polycomb complexes important for H3K4me3 and H3K27me3 deposition, respectively. Epigenetic profiling reveals a striking loss of H3K4me3, H3K27me3, and their associated enzymatic machinery at a significant subset of bivalent promoters in Dppa2/4 mutants, in addition to loss of H2A.Z and chromatin accessibility. In wild-type ESCs, these “Dppa2/4-dependent” bivalent promoters are characterised by low H3K4me3 enrichment and breadth, near-absent expression levels and initiating but not elongating RNA polymerase. Notably, Dppa2/4-dependent promoters are less evolutionarily conserved suggesting that they lack additional safeguard measures to maintain bivalency at these genes in the absence of Dppa2/4. Concomitantly with the loss of bivalency, Dppa2/4-dependent bivalent promoters gain DNA methylation and consequently are no longer able to be effectively activated upon ESC differentiation, leading to defects in cell fate acquisition. Our findings reveal a targeting principle for bivalency to developmental gene promoters poising them for future lineage specific gene activation.
2020-05-26 | PXD014981 | Pride
Project description:Dppa2 (Developmental pluripotency associated 2), specifically expressed in embryonic stem cells (ESCs) and reactivated in certain cancers, plays important roles in regulating the transition between pluripotency and differentiation. However, its involvement in the DNA damage response (DDR) of mouse ESCs (mESCs) has remained unclear. Here, we identify a surprising pro-apoptotic function for Dppa2 as a novel p53-interacting partner in mESCs. Dppa2 physically interacts with p53 and is transcriptionally repressed by p53 upon DNA damage. By comparing the effects of Dppa2 in p53+/+ and p53-/- mESCs, we find that Dppa2 promotes DNA damage-induced apoptosis (DIA) of mESCs in a p53-dependent manner. RNA-seq and chromatin immunoprecipitation followed by sequencing (ChIP-seq) reveal that Dppa2 and p53 co-repress genes involved in cell cycle regulation and self-renewal, which are highly expressed in ESCs. Mechanistically, Dppa2 recruits p53 to the enhancers of these co-repressed genes. Consequently, Dppa2 depletion significantly compromises p53’s binding intensity and alleviates transcriptional repression. Collectively, our findings uncover a novel mechanism of p53-mediated apoptosis achieved through cooperation with its ESC-specific partner, Dppa2, thereby highlighting a previously unappreciated tumor suppressor identity of Dppa2.
2025-07-12 | GSE301903 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE31581: ECAT15-2/Dppa2 deficient ESCs GSE31582: ECAT15-2/Dppa2 transgenic rescue into ECAT15-2/Dppa2 deficient ESCs GSE31583: Lung of ECAT15-2/Dppa2 deficient embryo at E18.5 Refer to individual Series
2011-10-16 | E-GEOD-31584 | biostudies-arrayexpress
Project description:Epigenetic priming factors establish a permissive epigenetic landscape which is not required until a later developmental or physiological time point, temporally uncoupling the presence of these factors with their phenotypic effects. One classic example of epigenetic priming is in the context of bivalent chromatin, found in pluripotent stem cells and early embryos at key developmental gene promoters marked by both activating-associated H3K4me3 and repressive-associated H3K27me3 histone modifications. It is currently unknown how these bivalent domains are targeted, or precisely how they impact on lineage commitment. Here we show that the small heterodimerising non-enzymatic DNA binding proteins Developmental Pluripotency Associated 2 (Dppa2) and 4 (Dppa4) act as epigenetic priming factors to establish bivalency at a subset of developmental genes. Dppa2/4 localise to the +1 nucleosome position of bivalent genes and while they are not required for pluripotency in embryonic stem cells (ESCs), double knockout cells fail to exit pluripotency and to differentiate efficiently, with delays in upregulating bivalently marked lineage genes. Proteomics reveal that Dppa2/4 interact on chromatin with members of the COMPASS and Polycomb complexes important for H3K4me3 and H3K27me3 deposition, respectively. Epigenetic profiling reveals a striking loss of H3K4me3, H3K27me3, and their associated enzymatic machinery at a significant subset of bivalent promoters in Dppa2/4 mutants, in addition to loss of H2A.Z and chromatin accessibility. In wild-type ESCs, these “Dppa2/4-dependent” bivalent promoters are characterised by low H3K4me3 enrichment and breadth, near-absent expression levels and initiating but not elongating RNA polymerase. Notably, Dppa2/4-dependent promoters are less evolutionarily conserved suggesting that they lack additional safeguard measures to maintain bivalency at these genes in the absence of Dppa2/4. Concomitantly with the loss of bivalency, Dppa2/4-dependent bivalent promoters gain DNA methylation and consequently are no longer able to be effectively activated upon ESC differentiation, leading to defects in cell fate acquisition. Our findings reveal a targeting principle for bivalency to developmental gene promoters poising them for future lineage specific gene activation.
2020-06-23 | GSE135841 | GEO