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Global Genome Conformational Programming during Neuronal Development by CTCF and nFGFR1 - The Genome Archipelago Model

ABSTRACT: Global Genome Conformational Programming during Neuronal Development by CTCF and nFGFR1 - The Genome Archipelago Model

PROVIDER: PRJNA644398 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12158523_1.fastq.gz	Fastqsanger.gz
	SRR12158523_2.fastq.gz	Fastqsanger.gz
	SRR12158524_1.fastq.gz	Fastqsanger.gz
	SRR12158524_2.fastq.gz	Fastqsanger.gz
	SRR12158525_1.fastq.gz	Fastqsanger.gz

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Global Genome Conformational Programming during Neuronal Development by CTCF and nFGFR1 - The Genome Archipelago Model

Project description:This study advances a topologically integrated genome archipelago model that undergoes extensive structural transformations through the formation of nFGFR1-associated Topologically Associated Domains (TADs), replacing CTCF TADs, during the development of the stem cells to neurons. The makeover of the TAD islands serves to recruit distinct ontogenic programs.

2020-09-30 | GSE153884 | GEO

Global Genome Conformational Programming during Neuronal Development Is Associated with CTCF and Nuclear FGFR1-The Genome Archipelago Model.

Project description:During the development of mouse embryonic stem cells (ESC) to neuronal committed cells (NCC), coordinated changes in the expression of 2851 genes take place, mediated by the nuclear form of FGFR1. In this paper, widespread differences are demonstrated in the ESC and NCC inter- and intra-chromosomal interactions, chromatin looping, the formation of CTCF- and nFGFR1-linked Topologically Associating Domains (TADs) on a genome-wide scale and in exemplary HoxA-D loci. The analysis centered on HoxA cluster shows that blocking FGFR1 disrupts the loop formation. FGFR1 binding and genome locales are predictive of the genome interactions; likewise, chromatin interactions along with nFGFR1 binding are predictive of the genome function and correlate with genome regulatory attributes and gene expression. This study advances a topologically integrated genome archipelago model that undergoes structural transformations through the formation of nFGFR1-associated TADs. The makeover of the TAD islands serves to recruit distinct ontogenic programs during the development of the ESC to NCC.

| S-EPMC7795191 | biostudies-literature

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

Expression data from P7 mouse cerebral cortex and hippocampus -CTCF Nex-Cre mediated conditional knockout

Project description:The CCCTC-binding factor (CTCF) is key to chromatin conformational changes that promote cellular diversity, but nothing is known about its role in neurons. Here we produced mice with a conditional knockout (cKO) of CTCF in postmitotic projection neurons, mostly in the dorsal telencephalon. 390 transcripts were expressed at significantly different levels between CTCF-deficient and control cortex and hippocampus. 14 Total samples were analyzed. Statistical analysis was performed by ANOVA, using the core probe sets defined by Affymetrix with the revision of the clustered Pcdhs. A list of genes showing a significant difference by Ctcf deletion was generated using a false discovery rate (FDR) <0.05 with a fold difference of < -1.2 or > 1.2 as a cutoff value.

2012-07-25 | E-GEOD-38673 | biostudies-arrayexpress

Expression data from P7 mouse cerebral cortex and hippocampus -CTCF Nex-Cre mediated conditional knockout

2012-07-26 | GSE38673 | GEO

Alcohol induced increases in sperm Histone H3 lysine 4 trimethylation correlate with increased placental CTCF occupancy and altered developmental programming

Project description:Using a mouse model, studies by our group reveal that paternal preconception alcohol intake affects offspring fetal-placental growth, with long-lasting consequences on adult metabolism. Here, we tested the hypothesis that chronic preconception male alcohol exposure impacts histone enrichment in sperm and that these changes are associated with altered developmental programming in the placenta. Using chromatin immunoprecipitation, we find alcohol-induced increases in sperm histone H3 lysine 4 trimethylation (H3K4me3) that map to promoters and presumptive enhancer regions enriched in genes driving neurogenesis and craniofacial development. Given the colocalization of H3K4me3 with the chromatin binding factor CTCF across both sperm and embryos, we next examined CTCF localization in the placenta. We find global changes in CTCF binding within placentae derived from the male offspring of alcohol-exposed sires. Furthermore, altered CTCF localization correlates with dysregulated gene expression across multiple gene clusters; however, these transcriptional changes only occur in male offspring. Finally, we identified a correlation between genomic regions exhibiting alcohol-induced increases in sperm H3K4me3 and increased CTCF binding in male placentae. Collectively, our analysis demonstrates that the chromatin landscape of sperm is sensitive to chronic alcohol exposure and that a subset of these affected regions exhibits increased placental CTCF enrichment.

2022-05-24 | GSE203189 | GEO

CTCF loss has limited effects on genome architecture in Drosophila despite critical regulatory functions.

Project description:Proteins co-purifying with recombinantly purified and N-terminally GFP-3C-tagged CTCF N-terminus (amino acids 1-293) produced in bacteria were identified by incubating the tagged bait with soluble nuclear protein extracts from 0-12h hour-old wildtype (OregonR strain) Drosophila melanogaster embryos.

2021-01-18 | PXD019487 | Pride

A distinct motif for numerous CTCF binding sites in the murine IgH locus

Project description:Our studies have revealed that a large class of CTCF binding sites – namely the upstream sites – conform neither to a conformational nor a local recombinase activating role. Their conserved spatial distances upstream of V gene segments suggests a possible role in insulating V gene segments from neighboring V gene segments. In any case, understanding the sequence determinants of CTCF binding to the murine IgH locus should facilitate future studies evaluating how IgH locus accessibility regulates CTCF binding as well as the functions that CTCF plays in regulating the recombinational accessibility of VH gene segments during B cell development.

2019-07-02 | GSE124153 | GEO

Bromodomain-dependent stage-specific male genome programming by Brdt

Project description:This SuperSeries is composed of the following subset Series: GSE39908: Bromodomain-dependent stage-specific male genome programming by Brdt [ChIP-Seq] GSE39909: Bromodomain-dependent stage-specific male genome programming by Brdt [Illumina BeadArray] Refer to individual Series

2012-08-30 | E-GEOD-39910 | biostudies-arrayexpress

CTCF cooperates with CtIP to drive homologous recombination repair of double-strand breaks

Project description:The pleiotropic CCCTC-binding factor (CTCF) plays a role in homologous recombination (HR) repair of DNA double-strand breaks (DSBs). However, the precise mechanistic role of CTCF in HR remains largely unclear. Here, we show that CTCF engages in DNA end resection, which is the initial, crucial step in HR, through its interactions with MRE11 and CtIP. Depletion of CTCF profoundly impairs HR and attenuates CtIP recruitment at DSBs. CTCF physically interacts with MRE11 and CtIP and promotes CtIP recruitment to sites of DNA damage. Subsequently, CTCF facilitates DNA end resection to allow HR, in conjunction with MRE11-CtIP. Notably, the zinc finger domain of CTCF binds to both MRE11 and CtIP and enables proficient CtIP recruitment, DNA end resection, and HR. The N-terminus of CTCF is able to bind to only MRE11 and its C-terminus is incapable of binding to MRE11 and CtIP, thereby resulting in compromised CtIP recruitment, DSB resection, and HR. Overall, this suggests an important function of CTCF in DNA end resection through the recruitment of CtIP at DSBs. Collectively, our findings identify a critical role of CTCF at the first control point in selecting the HR repair pathway

2019-11-12 | PXD014441 | Pride

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