Euarchontoglires
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB12300 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Comprehensive analysis of the human adipose epigenome by transcriptome, open chromatin and methylome sequencing studies.
2015-05-01 | E-MTAB-3181 | biostudies-arrayexpress
Project description:Transposable elements are increasingly appreciated as regulatory elements in early mammalian development, especially in cells which exhibit pluripotency. Mammalian primordial germ cells (PGCs) must exit latent pluripotency in a process termed determination before they are competent to differentiate and enter sex-specific developmental programs. Here, we find that determination is marked by large changes to the transposable element (TE) repertoire, a phenomenon driven by TRIM28, after which testicular and ovarian PGCs exhibit district transposable element repertoires. We find that loss of TRIM28 perturbs entry into determination as marked by expression of DAZL in a sex-specific manner, but does not result in a failure to downregulate markers of latent pluripotency, including SOX2 and NANOG in either sex. Despite downregulation of some early PGC markers, both ovarian and testicular PGCs fail to properly enter into their meiotic germ cell or prospermatogonial programs, respectively. Thus, we show that TRIM28-mediated reorganization of the TE repertoire is necessary to establish a PGC epigenome competent for proper germline commitment and gametogenesis.
2025-04-29 | GSE266173 | GEO
Project description:Transposable elements are increasingly appreciated as regulatory elements in early mammalian development, especially in cells which exhibit pluripotency. Mammalian primordial germ cells (PGCs) must exit latent pluripotency in a process termed determination before they are competent to differentiate and enter sex-specific developmental programs. Here, we find that determination is marked by large changes to the transposable element (TE) repertoire, a phenomenon driven by TRIM28, after which testicular and ovarian PGCs exhibit district transposable element repertoires. We find that loss of TRIM28 perturbs entry into determination as marked by expression of DAZL in a sex-specific manner, but does not result in a failure to downregulate markers of latent pluripotency, including SOX2 and NANOG in either sex. Despite downregulation of some early PGC markers, both ovarian and testicular PGCs fail to properly enter into their meiotic germ cell or prospermatogonial programs, respectively. Thus, we show that TRIM28-mediated reorganization of the TE repertoire is necessary to establish a PGC epigenome competent for proper germline commitment and gametogenesis.
2025-04-29 | GSE266172 | GEO
Project description:In mammals, extensive chromatin reorganization is essential for reprogramming terminally committed gametes to a totipotent state during preimplantation development. However, the global chromatin landscape and its dynamics in this period remain unexplored. Here we report a genome-wide map of accessible chromatin in mouse preimplantation embryos using an improved assay for transposase-accessible chromatin with high throughput sequencing (ATAC-seq) approach with CRISPR/Cas9-assisted mitochondrial DNA depletion. We show that despite extensive parental asymmetry in DNA methylomes, the chromatin accessibility between the parental genomes is globally comparable after major zygotic genome activation (ZGA). Accessible chromatin in early embryos is widely shaped by transposable elements and overlaps extensively with putative cis-regulatory sequences. Unexpectedly, accessible chromatin is also found near the transcription end sites of active genes. By integrating the maps of cis-regulatory elements and single-cell transcriptomes, we construct the regulatory network of early development, which helps to identify the key modulators for lineage specification. Finally, we find that the activities of cis-regulatory elements and their associated open chromatin diminished before major ZGA. Surprisingly, we observed many loci showing non-canonical, large open chromatin domains over the entire transcribed units in minor ZGA, supporting the presence of an unusually permissive chromatin state. Together, these data reveal a unique spatiotemporal chromatin configuration that accompanies early mammalian development. Mouse preimplantation embryos were obtained from crosses of C57BL/6N and DBA/2N. ATAC-seq was performed in these embryos at various stages in preimplantation development.
2016-06-15 | E-GEOD-66581 | biostudies-arrayexpress
Project description:In mammals, extensive chromatin reorganization is essential for reprogramming terminally committed gametes to a totipotent state during preimplantation development. However, the global chromatin landscape and its dynamics in this period remain unexplored. Here we report a genome-wide map of accessible chromatin in mouse preimplantation embryos using an improved assay for transposase-accessible chromatin with high throughput sequencing (ATAC-seq) approach with CRISPR/Cas9-assisted mitochondrial DNA depletion. We show that despite extensive parental asymmetry in DNA methylomes, the chromatin accessibility between the parental genomes is globally comparable after major zygotic genome activation (ZGA). Accessible chromatin in early embryos is widely shaped by transposable elements and overlaps extensively with putative cis-regulatory sequences. Unexpectedly, accessible chromatin is also found near the transcription end sites of active genes. By integrating the maps of cis-regulatory elements and single-cell transcriptomes, we construct the regulatory network of early development, which helps to identify the key modulators for lineage specification. Finally, we find that the activities of cis-regulatory elements and their associated open chromatin diminished before major ZGA. Surprisingly, we observed many loci showing non-canonical, large open chromatin domains over the entire transcribed units in minor ZGA, supporting the presence of an unusually permissive chromatin state. Together, these data reveal a unique spatiotemporal chromatin configuration that accompanies early mammalian development. Mouse 2-cell embryos were obtained from crosses of C57BL/6N x PWK for ChIP-seq samples.
2016-06-15 | E-GEOD-79935 | biostudies-arrayexpress
Project description:The oocyte epigenome plays critical roles in mammalian gametogenesis and embryogenesis. Yet, how it is established remains elusive. Here, we report that histone-lysine N-methyltransferase SETD2, an H3K36me3 methyltransferase, is a crucial regulator of the mouse oocyte epigenome. Deficiency in Setd2 leads to extensive alterations of the oocyte epigenome, including the loss of H3K36me3, failure in establishing the correct DNA methylome, invasion of H3K4me3 and H3K27me3 into former H3K36me3 territories and aberrant acquisition of H3K4me3 at imprinting control regions instead of DNA methylation. Importantly, maternal depletion of SETD2 results in oocyte maturation defects and subsequent one-cell arrest after fertilization. The preimplantation arrest is mainly due to a maternal cytosolic defect, since it can be largely rescued by normal oocyte cytosol. However, chromatin defects, including aberrant imprinting, persist in these embryos, leading to embryonic lethality after implantation. Thus, these data identify SETD2 as a crucial player in establishing the maternal epigenome that in turn controls embryonic development.
2019-05-01 | GSE112834 | GEO
Project description:Transcription factors (TFs) in concert with chromatin pathways stably reset transcriptional programs during differentiation. Yet we know little how local sites of chromatin reprogramming are specified and how the estimated 3000 TF encoded in mammalian genomes contribute to chromatin dynamics. To identify candidate TFs we developed an integrated computational approach (Epi-MARA) that models chromatin dynamics in terms of predicted transcription factor binding sites and show that it correctly predicts key TFs involved in epigenome reorganization. When applied to a time course of genome-wide H3 lysine 27 trimethylation (H3K27me3), a chromatin mark set by the Polycomb system, during neuronal differentiation of murine stem cells Epi-MARA predicted that the repressive transcription factor REST contributes to a gain of H3K27me3 at a subset of promoters during the transition from the stem to the progenitor state. To test this prediction we identified, genome-wide, the actual binding sites of REST and H3K27me3 during the differentiation in cells that are either wildtype or in which REST had been deleted. REST indeed localizes to a subset of sites that gain H3K27me3 in progenitors. Importantly, absence of REST in trans leads to a loss of H3K27me3 predominantly in the neuronal progenitor state and specifically at those regions where REST was bound. This function further requires REST binding sites in cis as their mutation leads to substantial loss of H3K27me3. Taken together we provide a novel approach to identify epigenome and TF crosstalk during cellular reprogramming and prove experimentally the prediction that REST acts as an important recruiter of Polycomb repression during early steps of neurogenesis. Dataset comprises of 15 ChIP-seq samples using chromatin from embryonic stem (ES) and neuronal progentor (NP) of wildtype and RESTko cells, which was immunoprecipitated, using antibodies against REST, H3K27me3, or Suz12
2012-09-04 | E-GEOD-27148 | biostudies-arrayexpress
Project description:Transposable elements are increasingly appreciated as regulatory elements in early mammalian development, especially in cells which exhibit pluripotency. Mammalian primordial germ cells (PGCs) must exit latent pluripotency in a process termed determination before they are competent to differentiate and enter sex-specific developmental programs. Here, we find that determination is marked by large changes to the transposable element (TE) repertoire, a phenomenon driven by TRIM28, after which testicular and ovarian PGCs exhibit district transposable element repertoires. We find that loss of TRIM28 perturbs entry into determination as marked by expression of DAZL in a sex-specific manner, but does not result in a failure to downregulate markers of latent pluripotency, including SOX2 and NANOG in either sex. Despite downregulation of some early PGC markers, both ovarian and testicular PGCs fail to properly enter into their meiotic germ cell or prospermatogonial programs, respectively. Thus, we show that TRIM28-mediated reorganization of the TE repertoire is necessary to establish a PGC epigenome competent for proper germline commitment and gametogenesis.
2025-04-29 | GSE266176 | GEO
Project description:Comprehensive analysis of the human adipose epigenome by transcriptome, open chromatin and methylome sequencing studies.
2015-05-01 | E-MTAB-3182 | biostudies-arrayexpress
Project description:We describe an assay for transposase-accessible chromatin using sequencing (ATAC-seq), based on direct in vitro transposition of sequencing adaptors into native chromatin, as a rapid and sensitive method for integrative epigenomic analysis. ATAC-seq captures open chromatin sites using a simple two-step protocol with 500–50,000 cells and reveals the interplay between genomic locations of open chromatin, DNA-binding proteins, individual nucleosomes and chromatin compaction at nucleotide resolution. We discovered classes of DNA-binding factors that strictly avoided, could tolerate or tended to overlap with the nucleosome. Using ATAC-seq maps of human CD4+ T cells from a proband obtained on consecutive days, we demonstrated the feasibility of analyzing an individual’s epigenome on a timescale compatible with clinical decision-making. We examined chromatin structure using ATAC-seq in 2 cell types (GM12878 cell line, purified CD4+ T cells).
2013-10-01 | E-GEOD-47753 | biostudies-arrayexpress