RNA interactions are essential for proper CTCF function
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA517076 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8487480.fastq.gz | Fastqsanger.gz | |||
| SRR8487490.fastq.gz | Fastqsanger.gz | |||
| SRR8487500_1.fastq.gz | Fastqsanger.gz | |||
| SRR8487500_2.fastq.gz | Fastqsanger.gz | |||
| SRR8487481.fastq.gz | Fastqsanger.gz |
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Project description:The function of the CCCTC-binding factor (CTCF) in the organization of the genome has become an important area of investigation, but the mechanisms by which CTCF dynamically contributes to genome organization are not clear. We previously discovered that CTCF binds to large numbers of endogenous RNAs, promoting its self-association. In this regard, we now report two independent features that disrupt CTCF association with chromatin: inhibition of transcription and disruption of CTCF-RNA interactions through mutations of two of its 11 zinc fingers which are not required for CTCF binding to its cognate DNA site: zinc finger-1 (ZF1) or -10 (ZF10). These mutations alter gene expression profiles as CTCF mutants lose their ability to form chromatin loops and thus, the ability to insulate chromatin domains as well as mediate CTCF long-range genomic interactions. Our results point to the importance of CTCF-mediated RNA interactions as a structural component of genome organization.
2019-09-12 | GSE125595 | GEO
Project description:Catalytic activity of the ISWI family of remodelers is critical for nucleosomal organization and transcription factor binding, including the insulator protein CTCF. To define which subcomplex mediates these diverse functions we phenotyped a panel of isogenic mouse stem cell lines each lacking one of six ISWI accessory subunits. Individual deletions of either CERF, RSF1, ACF, WICH or NoRC subcomplexes only moderately affect the chromatin landscape, while removal of the NURF-specific subunit BPTF leads to drastic reduction in chromatin accessibility and Snf2h ATPase localization around CTCF sites. While this reduces distances to the adjacent nucleosomes it only modestly impacts CTCF binding itself. In absence of accessibility, the insulator function of CTCF is nevertheless impaired resulting in lower occupancy of cohesin and cohesin-loading factors, and reduced insulation at these sites, highlighting the need of NURF-mediated remodeling for open chromatin and proper CTCF function. Our comprehensive analysis reveals a specific role for NURF in mediating Snf2h localization and chromatin opening at bound CTCF sites showing that local accessibility is critical for cohesin binding and insulator function.
2024-03-13 | PXD042945 | Pride
Project description:Every known SWI/SNF chromatin-remodeling complex incorporates an ARID DNA binding domain-containing subunit. Despite being a ubiquitous component of these complexes, physiological roles for this domain remain undefined. We screened an N-ethyl-N-nitrosurea (ENU) mutagenized library for ARID domain point mutations and generated an Arid1a/Baf250a hypomorphic allele. The mutant ARID1a (V1068G) protein is stably expressed at wild-type levels, and it is capable of assembling into a SWI/SNF complex with in vitro mononucleosome disruption activity. However, its capacity to bind DNA is lost. Consistent with defective DNA binding, mutant protein occupancy at known SWI/SNF target genes is decreased. Loss of DNA binding is associated with concurrent changes in SWI/SNF target gene expression. Mutant embryos manifest heart defects, fail to establish proper yolk sac vasculature, and exhibit hemorrhaging. As a result of these phenotypes, mutant embryos fail to establish proper circulation, culminating in ischemic arrest in utero between days 9.5 and 11.5. These data support a role for ARID1a-containing, BAF-A complexes in heart and extraembryonic vascular development, and indicate the ARID domain of ARID1a is essential in this regard. Hence, intrinsic ARID subunit-DNA interactions are required for normal SWI/SNF function in vivo. Four-condition experiment, wild-type vs Baf250a/Arid1a^V1068G/V1068G yolk sacs isolated at E8.5 and E9.5. Biological replicates: 3 per condition.
2012-01-15 | E-GEOD-32116 | biostudies-arrayexpress
Project description:The ubiquitously expressed transcription factor CTCF maintains higher-order chromatin structure in multiple cell types and species through well-established common mechanisms. Here we define a new role for CTCF in tissue-specific gene regulation revealed by serial examinations of genome-wide CTCF occupancy during red blood cell (RBC) differentiation of human CD34+ hematopoietic stem/progenitor cells (HSPCs). We identified 1753 dynamic, erythroid developmental stage-specific CTCF chromatin occupancy sites that occur through both direct DNA binding and indirectly via interactions with lineage-specific transcription factors. These dynamic sites display features of transcriptional enhancers, function as hubs of cis-regulatory elements (CREs) interactome, and are enriched for single nucleotide polymorphisms (SNPs) associated with RBC traits. Precise deletion of CTCF binding motifs from those dynamically bound sites alternated local CRE-interactions and disrupted erythropoiesis. Our study highlights novel, lineage-specific functions for CTCF and provides new insights into how genetic variation regulates erythropoiesis
2021-01-18 | GSE131054 | GEO
Project description:The ubiquitously expressed transcription factor CTCF maintains higher-order chromatin structure in multiple cell types and species through well-established common mechanisms. Here we define a new role for CTCF in tissue-specific gene regulation revealed by serial examinations of genome-wide CTCF occupancy during red blood cell (RBC) differentiation of human CD34+ hematopoietic stem/progenitor cells (HSPCs). We identified 1753 dynamic, erythroid developmental stage-specific CTCF chromatin occupancy sites that occur through both direct DNA binding and indirectly via interactions with lineage-specific transcription factors. These dynamic sites display features of transcriptional enhancers, function as hubs of cis-regulatory elements (CREs) interactome, and are enriched for single nucleotide polymorphisms (SNPs) associated with RBC traits. Precise deletion of CTCF binding motifs from those dynamically bound sites alternated local CRE-interactions and disrupted erythropoiesis. Our study highlights novel, lineage-specific functions for CTCF and provides new insights into how genetic variation regulates erythropoiesis
2021-01-18 | GSE131053 | GEO
Project description:The ubiquitously expressed transcription factor CTCF maintains higher-order chromatin structure in multiple cell types and species through well-established common mechanisms. Here we define a new role for CTCF in tissue-specific gene regulation revealed by serial examinations of genome-wide CTCF occupancy during red blood cell (RBC) differentiation of human CD34+ hematopoietic stem/progenitor cells (HSPCs). We identified 1753 dynamic, erythroid developmental stage-specific CTCF chromatin occupancy sites that occur through both direct DNA binding and indirectly via interactions with lineage-specific transcription factors. These dynamic sites display features of transcriptional enhancers, function as hubs of cis-regulatory elements (CREs) interactome, and are enriched for single nucleotide polymorphisms (SNPs) associated with RBC traits. Precise deletion of CTCF binding motifs from those dynamically bound sites alternated local CRE-interactions and disrupted erythropoiesis. Our study highlights novel, lineage-specific functions for CTCF and provides new insights into how genetic variation regulates erythropoiesis
2021-01-18 | GSE131052 | GEO
Project description:Dynamic CTCF occupancy during differentiation rewires cis-regulatory module interactions essential for development
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Project description:CTCF modulates Estrogen Receptor function through specific chromatin and nuclear matrix interactions
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Project description:The ubiquitously expressed transcription factor CTCF maintains higher-order chromatin structure in multiple cell types and species through well-established common mechanisms. Here we define a new role for CTCF in tissue-specific gene regulation revealed by serial examinations of genome-wide CTCF occupancy during red blood cell (RBC) differentiation of human CD34+ hematopoietic stem/progenitor cells (HSPCs). We identified 1753 dynamic, erythroid developmental stage-specific CTCF chromatin occupancy sites that occur through both direct DNA binding and indirectly via interactions with lineage-specific transcription factors. These dynamic sites display features of transcriptional enhancers, function as hubs of cis-regulatory elements (CREs) interactome, and are enriched for single nucleotide polymorphisms (SNPs) associated with RBC traits. Precise deletion of CTCF binding motifs from those dynamically bound sites alternated local CRE-interactions and disrupted erythropoiesis. Our study highlights novel, lineage-specific functions for CTCF and provides new insights into how genetic variation regulates erythropoiesis
2021-01-18 | GSE131324 | GEO
Project description:CCCTC-binding factor (CTCF) is a DNA-binding protein that plays important roles in chromatin organization, though the mechanism by which CTCF carries out these functions is not fully understood. Recent studies show that CTCF recruits the cohesin complex to insulator sites and that cohesin is required for insulator activity. Here we have shown that the DEAD box RNA helicase p68 (DDX5) and its associated noncoding RNA, steroid receptor RNA activator (SRA), form a complex with CTCF that is essential for insulator function. p68 was detected at CTCF sites in the IGF2/H19 imprinted control region (ICR) as well as other genomic CTCF sites. In vivo depletion of SRA or p68 reduced CTCF-mediated insulator activity at the IGF2/H19 ICR, increased levels of IGF2 expression, and increased interactions between the endodermal enhancer and IGF2 promoter. p68/SRA also interacts with members of the cohesin complex. Depletion of either p68 or SRA does not affect CTCF binding to its genomic sites, but it does reduce cohesin binding. The results suggest that p68/SRA stabilizes the interaction of cohesin with CTCF, by binding to both, and is required for proper insulator function. Identification of p68-binding sites in Hela cells using ChIP-Seq.
2010-11-16 | E-GEOD-24126 | biostudies-arrayexpress