Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CTCF and Cohesin (Rad21) ChIP-seq in male mouse liver

ABSTRACT: Sequencing files provided here include mouse liver ChIP-seq for CTCF and the cohesin subunit Rad21. These files are part of a larger study where we describe features of Topologically Associating Domains (TADs) and their impact on liver gene expression, then use these features to computationally predict subTAD structures not otherwise readily identifiable due to the low resolution of Hi-C. Our findings reveal that CTCF-based subTAD loops maintain key insulating properties of TADs, and support the proposal that subTADs are formed by the same loop extrusion mechanism and contribute to nuclear architecture as intra-TAD scaffolds that further constrain enhancer-promoter interactions. This allows high expression of super enhancer target genes and individual genes within inactive TADs, and may be a broadly conserved mechanism of genomic regulation.

ORGANISM(S): Mus musculus

PROVIDER: GSE102997 | GEO | 2018/05/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

4C-seq analysis of interactions with the Albumin promoter in mouse liver

Project description:Sequencing files provided here include mouse liver ChIP-seq for CTCF and the cohesin subunit Rad21, and 4C-seq analyses in male and female mouse liver centered at an Albumin promoter viewpoint. These files are part of a larger study where we describe features of Topologically Associating Domains (TADs) and their impact on liver gene expression, then use these features to computationally predict subTAD structures not otherwise readily identifiable due to the low resolution of Hi-C. Our findings reveal that CTCF-based subTAD loops maintain key insulating properties of TADs, and support the proposal that subTADs are formed by the same loop extrusion mechanism and contribute to nuclear architecture as intra-TAD scaffolds that further constrain enhancer-promoter interactions. This allows high expression of super enhancer target genes and individual genes within inactive TADs, and may be a broadly conserved mechanism of genomic regulation.

2018-05-11 | GSE102998 | GEO

Modeling of DNA methylation in cis reveals principles of chromatin folding in vivo in the absence of crosslinking and ligation

Project description:Mammalian chromosomes are folded into intricate hierarchies of interaction domains, within which topologically associating domains (TADs) and CTCF-associated loops partition the physical interactions between regulatory sequences. Current understanding of chromosome folding largely relies on chromosome conformation capture (3C)-based experiments, where chromosomal interactions are detected as ligation products after crosslinking of chromatin. To measure chromosome structure in vivo, quantitatively and without relying on crosslinking and ligation, we have implemented a modified version of damID named damC. DamC combines DNA-methylation based detection of chromosomal interactions with next-generation sequencing and a biophysical model of methylation kinetics. DamC performed in mouse embryonic stem cells provides the first in vivo validation of the existence of TADs and CTCF loops and confirms 3C-based measurements of the scaling of contact probabilities. Combining damC with transposon-mediated genomic engineering shows that new loops can be formed between ectopically introduced and endogenous CTCF sites, which alters the partitioning of physical interactions within TADs. This orthogonal approach to 3C provides the first crosslinking- and ligation-free validation of the existence of key structural features of mammalian chromosomes and provides novel insights into how chromosome structure within TADs can be manipulated.

2019-06-03 | PXD013507 | Pride

CTCF and Cohesin (Rad21) ChIP-seq in female mouse liver

Project description:Sequencing files provided here include mouse liver ChIP-seq for CTCF and the cohesin subunit Rad21. These files are part of a larger study ("CTCF and Cohesin link sex-biased distal regulatory elements to sex-biased gene expression in mouse liver") where we compare CTCF and cohesin binding in male and female mouse liver as well as differences in chromatin conformation (DNA looping).

2020-07-07 | GSE130908 | GEO

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [ChIP-Seq]

Project description:Epigenetic mechanisms often play an important role in driving tumor progression towards metastasis. It is less clear that deregulation of chromatin architecture, including topologically associated domains (TADS), contributes to cancer progression. CTCF is a central regulator of three dimensional chromatin structure that undergoes copy number loss in over half of all breast cancers, but the impact of this defect on epigenetic programming and chromatin architecture remains obscure. We find that the reduced pools of CTCF in hemizygous models potentiates cell invasion. Underlying this phenotype is the activation of oncogenic networks including the PI3K signaling cascade, which presents therapeutic vulnerabilities, especially to mTOR inhibitors. Deregulation of these oncogenic pathways is largely due to the loss of CTCF insulation, allowing a reorganization of long-range chromatin contacts at the subTAD level that is associated with aberrant programming of H3K27 acetylation at enhancer/promoter regions. Thus, lowered CTCF levels lead to chromatin reorganization facilitating pro-invasive transcriptional programs.

2022-01-01 | GSE183379 | GEO

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [Hi-C]

2022-01-01 | GSE183378 | GEO

3D Chromatin Remodeling Potentiates Transcriptional Programs Driving Cell Invasion [RNA-Seq]

2022-01-01 | GSE183380 | GEO

ChIP-seq analyses of CTCF binding in liver samples from CAST/EiJ and SPRET/EiJ (Mus spretus) mice, and of the cohesin subunit RAD21 in C57BL/6J mouse liver

Project description:We explored the relationship between the evolutionary dynamics of CTCF binding and the functional stability of higher order genome structures, by performing ChIP-seq experiments in closely related Mus species or strains and intersecting with Hi-C-derived topologically associating domains (TADs) and expression data. All experiments were performed in adult male liver samples in 3 biological replicates and with an input control set. We also generated RAD21 (cohesin subunit) ChIP-seq from a replicate of adult male mouse (C57BL/6J) liver to determine localization of cohesin with respect to CTCF.

2019-11-20 | E-MTAB-8014 | biostudies-arrayexpress

Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [Hi-C]

Project description:Antigen receptor loci are organized into variable (V), diversity (D), and joining (J) elements that rearrange to generate diverse antigen receptor repertoires. Here, we identified an enhancer (E34) in the immunoglobulin kappa locus (Igκ) that instructed rearrangement of Vκ genes located in a sub-topologically associating domain (subTAD), including a Vκ gene encoding for antibodies targeting bacterial phosphorylcholine. E34 promoted the deposition of active histone marks across the E34 subTAD to instruct its nuclear repositioning from a V(D)J recombination-repressive compartment to a permissive one. E34-induced nuclear repositioning of the E34 subTAD promoted Vκ-Jκ interactions assisted by enhancer-associated epigenetic marks and de novo CTCF binding. Finally, we found that E34-instructed Vκ-Jκ rearrangement was essential to combat Streptococcus pneumoniae but not methicillin-resistant Staphylococcus aureus or influenza infections. These data show how enhancer-instructed chromatin topology mechanically pulls specific Vκ and Jκ genes into close physical proximity to generate distinct antibody repertoires to combat bacterial infection.

2022-12-05 | GSE193967 | GEO

Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [RNA-seq]

2022-12-05 | GSE193846 | GEO

Enhancer-instructed chromatin folding and compartmentalization dictate Vκ repertoire rearrangement to combat bacterial infection [CUT&RUN]

2022-12-05 | GSE193822 | GEO