Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA305313 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Mouse embryonic stem cells are heterogeneous and contain rare cells expressing transcripts normally upregulated in pre-implantation embryos, including the Zscan4 cluster and MuERVL endogenous retrovirus. Through single cell transcriptomics and genome-wide chromatin and DNA methylation analyses we uncover the dynamics of the regulation and epigenetic consequences of these transient cells. Transcriptional activation of MuERVL and Zscan4 coincided with a global increase in chromatin accessibility. Through a combination of bulk and single-cell RNA-sequencing, we reveal the dynamics and specificities of a MuERVL driven transcriptional network. Interestingly, in addition to pre-implantation embryos, the MuERVL network is similarly upregulated during somatic cell reprogramming, associating it with dramatic chromatin remodeling events. In MuERVL+ mESCs, upregulation of a cluster of Eif1A-like genes results in inhibition of protein synthesis, uncoupling transcription from translation. Consequently, depletion of proteins including DNA methyltransferases, results in genome-wide DNA demethylation, demonstrating the influence of endogenous retroviral activation on the host epigenome.
2016-10-03 | GSE85776 | GEO
Project description:Mouse embryonic stem cells are heterogeneous and contain rare cells expressing transcripts normally upregulated in pre-implantation embryos, including the Zscan4 cluster and MuERVL endogenous retrovirus. Through single cell transcriptomics and genome-wide chromatin and DNA methylation analyses we uncover the dynamics of the regulation and epigenetic consequences of these transient cells. Transcriptional activation of MuERVL and Zscan4 coincided with a global increase in chromatin accessibility. Through a combination of bulk and single-cell RNA-sequencing, we reveal the dynamics and specificities of a MuERVL driven transcriptional network. Interestingly, in addition to pre-implantation embryos, the MuERVL network is similarly upregulated during somatic cell reprogramming, associating it with dramatic chromatin remodeling events. In MuERVL+ mESCs, upregulation of a cluster of Eif1A-like genes results in inhibition of protein synthesis, uncoupling transcription from translation. Consequently, depletion of proteins including DNA methyltransferases, results in genome-wide DNA demethylation, demonstrating the influence of endogenous retroviral activation on the host epigenome.
2016-10-01 | GSE75751 | GEO
Project description:Genome-wide DNA demethylation is a unique feature of mammalian development and naïve pluripotent stem cells. So far, it was unclear how mammals specifically achieve global DNA hypomethylation, given the high conservation of the DNA (de-)methylation machinery among vertebrates. We found that DNA demethylation requires TET activity but mostly occurs at sites where TET proteins are not bound suggesting a rather indirect mechanism. Among the few specific genes bound and activated by TET proteins was the naïve pluripotency and germline marker Dppa3 (Pgc7, Stella), which undergoes TDG dependent demethylation. The requirement of TET proteins for genome-wide DNA demethylation could be bypassed by ectopic expression of Dppa3. We show that DPPA3 binds and displaces UHRF1 from chromatin and thereby prevents the recruitment and activation of the maintenance DNA methyltransferase DNMT1. We demonstrate that DPPA3 alone can drive global DNA demethylation when transferred to amphibians (Xenopus) and fish (medaka), both species that naturally do not have a Dppa3 gene and exhibit no post-fertilization DNA demethylation. Our results show that TET proteins are responsible for active and - indirectly also for - passive DNA demethylation; while TET proteins initiate local and gene-specific demethylation in vertebrates, the recent emergence of DPPA3 introduced a unique means of genome-wide passive demethylation in mammals and contributed to the evolution of epigenetic regulation during early mammalian development.
2020-10-12 | PXD019794 | Pride
Project description:Genome-wide DNA demethylation, including the erasure of genome imprints, in primordial germ cells (PGCs), is critical as a first step for creating the totipotent epigenome in the germ line. Here, we provide evidence that contrary to the prevailing model involving active DNA demethylation, imprint erasure in mouse PGCs occurs in a manner consistent with replication-coupled passive DNA demethylation: PGCs erase imprints during their rapid proliferation with little de novo as well as maintenance DNA methylation potential and no major chromatin alterations. Our findings necessitate the re-evaluation of and provide novel insights into the mechanism of genome-wide DNA demethylation in PGCs.
2013-03-04 | GSE40412 | GEO
Project description:Rif1 Promotes a Repressive Chromatin State to Safeguard Against Endogenous Retrovirus Activation
| PRJNA384427 | ENA
Project description:Here we report Human Endogenous Retrovirus 1 (HERV1-env) induction of endoplasmic reticulum (ER) stress with Unfolded Protein Response (UPR) activation, through its interaction with ATF6.ATF6α up-regulates RORC, STAT3 and TBX21 and induces IL-17A and INF-γ production in Tregs by binding to promoter sequences.
2022-08-02 | GSE135410 | GEO
Project description:Zygotic genome activation (ZGA) occurs at the mid-blastula transition (MBT) in zebrafish and is a period of chromatin remodeling. Genome-scale gametic demethylation and remethylation occurs after fertilization, during blastula stages, but how ZGA relates to promoter DNA methylation states is unknown. Using methylated DNA immunoprecipitation coupled to high-density microarray hybridization (MeDIP-ChIP), we characterize genome-wide promoter DNA methylation dynamics before, during and after ZGA onset, in relation changes in post-translational histone modification and gene expression (Series GSE22830). A Kolmogorov-Smirnov (KS) test was applied with P <= 0.01 to identify methylation peaks.
2012-07-06 | GSE33236 | GEO
Project description:We report that the winged helix transcription factor FOXA1 is unexpectedly associated with components of single and double stranded-DNA repair complexes. Biochemical studies and high-throughput approaches validated the hierarchical composition of this FOXA1-nucleated machinery and revealed the dependency on FOXA1 for global targeting of the key repair polymerase POLB. Genome-wide DNA methylomes at single-base resolution demonstrated that FOXA1-DNA repair complex is functionally linked to DNA demethylation in a lineage specific fashion. Loss-of-function studies indicate that a significant portion of FOXA1-bound regions display localized reestablishment of methylation and that the subsets with most consistent hypermethylation are represented by active promoters and enhancers that also exhibit the greatest depletion of POLB following FOXA1 removal. Consistently, forced expression of FOXA1 commits its binding sites to an active DNA demethylation in a POLB dependent manner. Finally, we showed that FOXA1-associated DNA demethylation is tightly coupled with genomic targeting of estrogen receptor and estrogen responsiveness. Together, our results link FOXA1-associated DNA demethylation to its transcriptional pioneering.
2016-06-08 | PXD004271 | Pride
Project description:Rif1 Promotes a Repressive Chromatin State to Safeguard Against Endogenous Retrovirus Activation [ChIP-seq]
| PRJNA384441 | ENA
Project description:Rif1 Promotes a Repressive Chromatin State to Safeguard Against Endogenous Retrovirus Activation [ATAC-seq]
| PRJNA384443 | ENA