Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA245416 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1262950_1.fastq.gz | Fastqsanger.gz | |||
| SRR1262950_2.fastq.gz | Fastqsanger.gz | |||
| SRR1262960_1.fastq.gz | Fastqsanger.gz | |||
| SRR1262960_2.fastq.gz | Fastqsanger.gz | |||
| SRR1262970_1.fastq.gz | Fastqsanger.gz |
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Project description:Heterochromatin is required to restrict aberrant expression of retrotransposons, but it remains poorly defined due to the underlying repeat-rich sequences. We dissected Suv39h-dependent histone H3 lysine 9 trimethylation (H3K9me3) by genome-wide ChIP-sequencing in mouse embryonic stem cells (ESCs). Refined bioinformatic analyses of repeat subfamilies indicated selective accumulation of Suv39h-dependent H3K9me3 at interspersed repetitive elements that cover ~ 5% of the ESC epigenome. The majority of the ~ 8,150 intact long interspersed nuclear elements (LINEs) and endogenous retroviruses (ERVs), but only a minor fraction of the > 1.8 million degenerate and truncated LINEs/ERVs, are enriched for Suv39h-dependent H3K9me3. Transcriptional repression of these intact LINEs and ERVs is differentially regulated by Suv39h and other chromatin modifiers in ESCs but governed by DNA methylation in committed cells. These data provide a novel function for Suv39h-dependent H3K9me3 chromatin to specifically repress intact retrotransposon elements in the ESC epigenome. ChIP-seq and RNA-seq in mouse ES cells, Neural precursors and MEFs wild type and Suv39h double KO. The input for ES cells is accessioned as GSM1251941. A link to this sample can be found below.
2014-06-26 | E-GEOD-57092 | biostudies-arrayexpress
Project description:Heterochromatin is required to restrict aberrant expression of retrotransposons, but it remains poorly defined due to the underlying repeat-rich sequences. We dissected Suv39h-dependent histone H3 lysine 9 trimethylation (H3K9me3) by genome-wide ChIP-sequencing in mouse embryonic stem cells (ESCs). Refined bioinformatic analyses of repeat subfamilies indicated selective accumulation of Suv39h-dependent H3K9me3 at interspersed repetitive elements that cover ~ 5% of the ESC epigenome. The majority of the ~ 8,150 intact long interspersed nuclear elements (LINEs) and endogenous retroviruses (ERVs), but only a minor fraction of the > 1.8 million degenerate and truncated LINEs/ERVs, are enriched for Suv39h-dependent H3K9me3. Transcriptional repression of these intact LINEs and ERVs is differentially regulated by Suv39h and other chromatin modifiers in ESCs but governed by DNA methylation in committed cells. These data provide a novel function for Suv39h-dependent H3K9me3 chromatin to specifically repress intact retrotransposon elements in the ESC epigenome.
2014-06-26 | GSE57092 | GEO
Project description:Reprogramming of H3K9me3-dependent heterochromatin is required for early development. How H3K9me3 is involved in early human development is, however, largely unclear. Here, we resolve the temporal landscape of H3K9me3 during human preimplantation development and its regulation for diverse hominoid-specific retrotransposons. At the 8-cell stage, H3K9me3 reprogramming at hominoid-specific retrotransposons termed SINE-VNTR-Alu (SVA) facilitates interaction between certain promoters and SVA-derived enhancers, facilitating the zygotic genome activation. In trophectoderm, de novo H3K9me3 domains prohibit pluripotent transcription factors from binding on hominoid-specific retrotransposons-derived regulatory elements for inner cell mass (ICM)-specific genes. H3K9me3 re-establishment at SVA elements in ICM is associated with higher transcription of DNA damage repair genes, compared to naïve human pluripotent stem cells. Our data demonstrate that species-specific reorganization of H3K9me3-dependent heterochromatin at hominoid-specific retrotransposons plays important roles during early human development, shedding light on how the epigenetic regulatory network for early development has evolved in mammals.
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Project description:In mammals, many germline genes are repressed by epigenetic mechanisms to prevent their illegitimate expression in embryonic and somatic cells. To advance our understanding of the complete mechanisms restricting the expression of germline genes in mammals, we analyzed the chromatin signature of germline genes and performed a genome-wide CRISPR-Cas9 knock-out screen for genes involved in germline gene repression using a reporter system in which GFP is under the control of the epigenetically repressed Dazl germline promoter in mouse embryonic stem cells (ESCs). We showed that the repression of germline genes mainly depends on the polycomb complex PRC1.6 and DNA methylation, which function additively in mouse ESCs. Furthermore, we identified and validated several novel genes involved in the repression of germline genes, and characterized three of them: Usp7, Shfm1 (also known as Sem1) and Erh. Inactivation of Usp7, Shfm1 or Erh led to the upregulation of germline genes, as well as retrotransposons for Shfm1, in mouse ESCs. Functionally, Usp7 acts at two levels: firstly it associates with PRC1.6 components and represses germline genes independently of DNA methylation, and secondly it facilitates DNA methylation deposition at germline genes for long term repression. In summary, our study provides a global view of the epigenetic mechanisms and novel factors required for silencing germline genes in embryonic cells.
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Project description:Heterochromatin plays essential roles in repressing retrotransposons, e.g. endogenous retroviruses (ERVs) during mammalian development, but the contribution of retrotransposition to lethality observed in embryonic cells deficient for heterochromatin-mediated ERV repression is poorly understood. Here we report that selective degradation of the TRIM28 heterochromatin adapter protein leads to reduced association of transcriptional condensates with loci encoding super-enhancer -driven pluripotency genes in embryonic stem cells, a collapse of the pluripotency transcriptional circuit, and a pre-lethal restriction of pluripotent lineages in mouse embryos. De-repressed ERVs recruit transcriptional condensates in the absence of TRIM28, and ERV RNA facilitates condensation of RNA Polymerase II in vitro. We propose that retrotransposons contribute to the genomic distribution of nuclear condensates, and that RNA species may facilitate “hijacking” of transcriptional condensates in various developmental and disease contexts.
2022-07-08 | PXD021895 | Pride
Project description:SETDB1 is a histone methyltransferase with essential roles in mouse development. It mediates transcriptional repression of genes and repetitive elements in different cell-types by depositing histone H3 lysine 9 trimethylation (H3K9me3). However, the function of differential H3K9me3 enrichment between cell- and tissue-types remains unclear. In this study, we demonstrate a global mutual exclusivity of H3K9me3 and CTCF across mouse tissues from different developmental time points. To investigate the mechanistic relationship, we analyzed SETDB1 depleted mouse embryonic stem cells and discovered that H3K9me3 prevents aberrant CTCF binding independently of DNA methylation and H3K9me2. Such sites are enriched with retrotransposons such as SINE B2 elements, which are not previously defined as targets of SETDB1. While the epigenetic modifier is known to silence transcriptional enhancers, its effects on higher-order chromatin structures have not been clearly defined. Overall, large chromatin structures including topologically associated domains and subnuclear compartments, remain intact. However, chromatin loops and local interactions are disrupted. Such perturbations lead to transcriptional changes by altering pre-existing chromatin landscapes, where specific genes have differential interactions with dysregulated cis-regulatory elements. This mode of transcriptional regulation is distinct from the direct repression of genic promoters or enhancers. Collectively, we find that cell-type specific targets of SETDB1 contributes to maintaining cellular identities through shaping genome architecture and transcriptomic networks by modulating CTCF binding, representing a novel function for SETDB1 and H3K9me3.
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