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Maintenance of CTCF and transcription factor-mediated interactions from gametes to the early mouse embryo (Hi-C)

ABSTRACT: Maintenance of CTCF and transcription factor-mediated interactions from gametes to the early mouse embryo (Hi-C)

PROVIDER: PRJNA480450 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7504565_1.fastq.gz	Fastqsanger.gz
	SRR7504565_2.fastq.gz	Fastqsanger.gz
	SRR7504566_1.fastq.gz	Fastqsanger.gz
	SRR7504566_2.fastq.gz	Fastqsanger.gz
	SRR7634032_1.fastq.gz	Fastqsanger.gz

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Maintenance of CTCF and transcription factor-mediated interactions from gametes to the early mouse embryo (Hi-C)

Project description:Mechanisms by which the mammalian gametes encode epigenetic information that can be transmitted to the progeny are relatively unknown. We find that many sperm promoters in mouse sperm are occupied by phosphorylated forms of RNA polymerase II and the Mediator complex. Analysis of ATAC-seq data suggest that the same promoters are occupied by components of the transcription complex in GV and MII oocytes and preimplantation embryos. Furthermore, distal ATAC-seq sites containing transcription factor motifs are conserved in monkeys and humans. ChIP-seq analyses confirm that transcription factors, including FoxA1 and the androgen and estrogen receptors, occupy distal enhancers. These sites and their interactions with promoters in the gametes are maintained in the early embryo. Additionally, sperm- or oocyte-specific interactions mediated by CTCF/cohesin are only present in the paternal or maternal chromosome, respectively in the zygote and 2-cell stages. These interactions converge in both chromosomes by the 8-cell stage. These results suggest that the mammalian gametes contain a large repertoire of transcription factors that organize a complex pattern of 3D interactions and can be transmitted to the zygote after fertilization.

2019-02-28 | GSE116856 | GEO

Maintenance of CTCF and transcription factor-mediated interactions from gametes to the early mouse embryo

Project description:Maintenance of CTCF and transcription factor-mediated interactions from gametes to the early mouse embryo

| PRJNA480443 | ENA

Maintenance of CTCF and transcription factor-mediated interactions from gametes to the early mouse embryo (ChIP-seq)

Project description:Maintenance of CTCF and transcription factor-mediated interactions from gametes to the early mouse embryo (ChIP-seq)

| PRJNA480447 | ENA

Maintenance of CTCF and transcription factor-mediated interactions from gametes to the early mouse embryo (ATAC-seq)

Project description:Maintenance of CTCF and transcription factor-mediated interactions from gametes to the early mouse embryo (ATAC-seq)

| PRJNA480448 | ENA

Maintenance of CTCF and transcription factor-mediated interactions from gametes to the early mouse embryo (ChIP-seq)

2019-02-28 | GSE116855 | GEO

Maintenance of CTCF and transcription factor-mediated interactions from gametes to the early mouse embryo (ATAC-seq)

2019-02-28 | GSE116854 | GEO

Maintenance of CTCF- and Transcription Factor-Mediated Interactions from the Gametes to the Early Mouse Embryo.

Project description:The epigenetic information present in mammalian gametes and whether it is transmitted to the progeny are relatively unknown. We find that many promoters in mouse sperm are occupied by RNA polymerase II (Pol II) and Mediator. The same promoters are accessible in GV and MII oocytes and preimplantation embryos. Sperm distal ATAC-seq sites containing motifs for various transcription factors are conserved in monkeys and humans. ChIP-seq analyses confirm that Foxa1, ERα, and AR occupy distal enhancers in sperm. Accessible sperm enhancers containing H3.3 and H2A.Z are also accessible in oocytes and preimplantation embryos. Furthermore, their interactions with promoters in the gametes persist during early development. Sperm- or oocyte-specific interactions mediated by CTCF and cohesin are only present in the paternal or maternal chromosomes, respectively, in the zygote and 2-cell stages. These interactions converge in both chromosomes by the 8-cell stage. Thus, mammalian gametes contain complex patterns of 3D interactions that can be transmitted to the zygote after fertilization.

| S-EPMC6625867 | biostudies-literature

Comparative Hi-C reveals that CTCF underlies evolution of chromosomal domain architecture.

Project description:Topological domains are key architectural building blocks of chromosomes in complex genomes. Their functional importance and evolutionary dynamics are however not well defined. Here we performed comparative Hi-C in liver cells from four mammalian species, and characterized the conservation and divergence of chromosomal contact insulation and the resulting domain architectures within distantly related genomes. We show that the modular organization of chromosomes is robustly conserved in syntenic regions. This overall conservation is compatible with conservation of the binding landscape of the insulator protein CTCF. Specifically, conserved CTCF sites are co-localized with cohesin, enriched at strong topological domain borders and bind to DNA motifs with orientations that define the directionality of CTCF’s long-range interactions. Interestingly, CTCF binding sites which are divergent between species are strongly correlated with divergence of internal domain structure. This divergence is likely driven by local CTCF binding sequence changes, demonstrating how genome evolution can be linked directly with a continuous flux of local chromosome conformation changes. Conversely, we provide evidence that large-scale domains are harder to break and that they are reorganized during genome evolution as intact modules. Hi-C and 4C-seq experiments were conducted in primary liver cells obtained from mouse, rabbit, macaque and dog

2015-02-26 | E-GEOD-65126 | biostudies-arrayexpress

Acute depletion of CTCF rewires genome-wide chromatin accessibility

Project description:The transcription factor CTCF appears indispensable in defining topologically associated domain boundaries and maintaining chromatin loop structures within these domains, supported by numerous functional studies. However, acute depletion of CTCF globally reduces chromatin interactions but does not significantly alter transcription. Here we systematically integrated multi-omics data including ATAC-seq, RNA-seq, WGBS, Hi-C, Cut&Run, CRISPR-Cas9 survival dropout screening, time-solved deep proteomic and phosphoproteomic analyses in cells carrying auxin-induced degron at endogenous CTCF locus. Acute CTCF protein degradation markedly rewired genome-wide chromatin accessibility. Increased accessible chromatin regions were largely located adjacent to CTCF-binding sites at promoter regions and insulator sites and were associated with enhanced transcription of nearby genes. In addition, we used CTCF-associated multi-omics data to establish a combinatorial data analysis pipeline to discover CTCF co-regulatory partners in regulating downstream gene expression. We successfully identified 40 candidates, including multiple established partners (i.e., MYC) supported by all layers of evidence. Interestingly, many CTCF co-regulators (e.g., YY1, ZBTB7A) that have evident alterations of respective downstream gene expression do not show changes at their expression levels across the multi-omics measurements upon acute CTCF loss, highlighting the strength of our system to discover hidden co-regulatory partners associated with CTCF-mediated transcription. This study highlights CTCF loss rewires genome-wide chromatin accessibility, which plays a critical role in transcriptional regulation

2021-07-04 | PXD026484 | Pride

Hi-C in Drosophila embryos at NC14 depleted of Beaf-32, CP190 or CTCF using the Bridge Adaptor Protocol

Project description:Hi-C was performed using the Bridge Adaptor Protocol in 2 biological replicates of Drosophila embryos at NC14 depleted of the maternal deposition of Beaf-32, CP190 or CTCF mRNA and protein. Embryos were collected at 2-3h AEL and were derived from mothers expressing RNAi against Beaf-32 or CP190 in the germline, or were genetic null for the maternal and zygotic contribution of CTCF.

2022-12-17 | E-MTAB-9158 | biostudies-arrayexpress

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