Genome-wide Chromatin Accessibility and Sequencing of HPEKs
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA554676 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12119159_1.fastq.gz | Fastqsanger.gz | |||
| SRR12119159_2.fastq.gz | Fastqsanger.gz | |||
| SRR12119160_1.fastq.gz | Fastqsanger.gz | |||
| SRR12119160_2.fastq.gz | Fastqsanger.gz | |||
| SRR12119161_1.fastq.gz | Fastqsanger.gz |
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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
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Project description:Differential accessibility of DNA to nuclear proteins underlies the regulation of numerous cellular processes. DNA accessibility is primarily determined by the presence or absence of nucleosomes. At present, methods for mapping the positions and occupancy of nucleosomes genome-wide (MNase-seq) have uncovered the nucleosomal landscapes of different cell types and organisms. Conversely, methods specialized for the detection of large nucleosome-free regions of chromatin (DNase-seq, FAIRE-seq) have uncovered numerous gene regulatory elements. However, these methods are less successful in measuring the accessibility of DNA sequences within nucelosome arrays. Here we describe a new genome-wide method, RED-seq (deep sequencing analysis of Restriction Enzyme Digestion), that measures chromatin accessibility in an unbiased way. Using this method, we identified differences in chromatin accessibility between populations of cells, not only in broadly nucleosome-depleted regions of the genome (e.g., enhancers and promoters), but also within the more widespread regions of nucleosomal occupancy. Furthermore, RED-seq identified both large differences in chromatin accessibility in distinct cell lineages and subtle changes observed during differentiation of mouse embryonic stem cells (ESCs). Most notably, using RED-seq, we detected differences in accessibility among sequences occupied by distinct nucleosome variants. Therefore, RED-seq provides unique insights into genome-wide chromatin dynamics.
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Project description:Genome-wide chromatin state underlies gene expression potential and cellular function. Epigenetic features and nucleosome positioning contribute to the accessibility of DNA, but widespread regulators of chromatin state are largely unknown. Our study investigates how coordination of ANP32E and H2A.Z contributes to genome-wide chromatin state in mouse fibroblasts. We define H2A.Z as a universal chromatin accessibility factor, and demonstrate that ANP32E antagonizes H2A.Z accumulation to restrict chromatin accessibility genome-wide. In the absence of ANP32E, H2A.Z accumulates at promoters in a hierarchical manner. H2A.Z initially localizes downstream of the transcription start site, and if H2A.Z is already present downstream, additional H2A.Z accumulates upstream. This hierarchical H2A.Z accumulation coincides with improved nucleosome positioning, heightened transcription factor binding, and increased expression of neighboring genes. Thus, ANP32E dramatically influences genome-wide chromatin accessibility through subtle refinement of H2A.Z patterns, providing a means to reprogram chromatin state and to hone gene expression levels.
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Project description:Genome-wide chromatin state underlies gene expression potential and cellular function. Epigenetic features and nucleosome positioning contribute to the accessibility of DNA, but widespread regulators of chromatin state are largely unknown. Our study investigates how coordination of ANP32E and H2A.Z contributes to genome-wide chromatin state in mouse fibroblasts. We define H2A.Z as a universal chromatin accessibility factor, and demonstrate that ANP32E antagonizes H2A.Z accumulation to restrict chromatin accessibility genome-wide. In the absence of ANP32E, H2A.Z accumulates at promoters in a hierarchical manner. H2A.Z initially localizes downstream of the transcription start site, and if H2A.Z is already present downstream, additional H2A.Z accumulates upstream. This hierarchical H2A.Z accumulation coincides with improved nucleosome positioning, heightened transcription factor binding, and increased expression of neighboring genes. Thus, ANP32E dramatically influences genome-wide chromatin accessibility through subtle refinement of H2A.Z patterns, providing a means to reprogram chromatin state and to hone gene expression levels.
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Project description:A genome wide screening for effectors of chromatin accessibility
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Project description:Acute depletion of CTCF rewires genome-wide chromatin accessibility
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Project description:Accumulated data suggest that transcription factor CTCF is indispensable to define topologically associated domain (TAD) boundaries and to maintain intra-TAD chromatin loop structures. However, upon genome-wide acute depletion of CTCF, the discrepancy between global reduction of chromatin interactions and minimal alteration of transcription has been evidently observed. To understand CTCF’s direct role in chromatin accessibility and global transcriptional regulation, we have systematically integrated data collected from ATAC-seq, RNA-seq, whole genome bisulfite-seq, Cut&Run and HiC in a previously established CTCF-miniAID knock-in cell lines. Acute degradation of CTCF markedly rewires genome-wide chromatin accessibility but not DNA methylation. Differentially altered ATAC-seq peaks are highly associated with adjacent CTCF binding sites, supporting the direct link between CTCF occupancy and its surrounding chromatin accessibility. Increased ATAC-seq peaks upon CTCF loss are notably associated with enhanced transcription at promoter regions and insulator sites, while decreased ATAC-seq peaks are significantly enriched at DNA loops. Furthermore, using CTCF associated multi-Omics data we have established a combinatorial data analysis pipeline to discover novel CTCF mediated insulators in the genome, by which we have successfully identified 67 novel insulators at non-coding regions distal to promoters. Functional CRISPR interference (CRISPRi) unconstrained the repressive transcriptional regulation of target genes. In sum, using CTCF acute depletion cell model and multi-Omics analysis, we concluded that CTCF loss rewires genome-wide chromatin accessibility, which plays a critical role for transcriptional regulation.
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Project description:To study the chromatin accessibility across the genome of DIPG-VII, DIPG-IV, and DIPG-XIII cell lines, we performed ATACseq (Assay for Transposase-Accessible Chromatin with high-throughput sequencing).
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Project description:Genome-wide Chromatin Accessibility is Restricted by ANP32E [CUT&Tag]
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