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CTCF tunes gene expression in a loop-dependent and -independent manner [ChIP-Seq]

ABSTRACT: ChIP experiments were performed to investigate the changes of CTCF and several chromatin remodeling subunits following CTCF degradation in mouse embryonic stem cells and found that acute CTCF degradation reduced the binding of CHD4 and CHD8.

ORGANISM(S): Mus musculus

PROVIDER: GSE274792 | GEO | 2026/05/06

REPOSITORIES: GEO

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CTCF tunes gene expression in a loop-dependent and -independent manner [ATAC-Seq]

Project description:This study was aimed to investigate the influence of CTCF degradation on chromatin accessibility, and discovered that CTCF loss reduced chromatin accessbility

2026-05-06 | GSE274789 | GEO

CTCF tunes gene expression in a loop-dependent and -independent manner [RNA-seq]

Project description:In this study, we aimed to investigate changes in gene expression following CTCF degradation, and found that CTCF primarily regulated gene expression in a loop-independent manner when it bound at gene promoters.

2026-05-06 | GSE274773 | GEO

CTCF tunes gene expression in a loop-dependent and -independent manner [Hi-C]

Project description:BL-Hi-C was performed in CTCF AID cells with or without overexpression of wild-type or Y226A/F228A double mutant CTCF to verify that mutant CTCF cannot mediate significant chromatin loops.

2026-05-06 | GSE274884 | GEO

CTCF tunes gene expression in a loop-dependent and -independent manner [MNase HiChIP]

Project description:CTCF, RAD21 and H3K27ac MNase HiChIP experiments were performed to capture their mediated chromatin interactions. Our data showed that the change in H3K27ac mediated chromatin interactions was minimal upon acute CTCF loss.

2026-05-06 | GSE274794 | GEO

CTCF tunes gene expression in a loop-dependent and -independent manner [TT-seq]

Project description:By using TT-seq, we investigated whether CTCF regulated gene expression by repressing antisense transcription. Our results showed that only few genes were regulated in this way, and CTCF might exert its loop-independent regulatory role through other mechanisms.

2026-05-06 | GSE274797 | GEO

CTCF tunes gene expression in a loop-dependent and -independent manner [MNase-based 4C-seq]

Project description:By designing specific primers targeting different genomic loci, M4C was used to capture chromatin interactions mediated by these loci and to reveal the changes in chromatin interactions upon acute CTCF loss.

2026-05-06 | GSE274799 | GEO

CTCF tunes gene expression in a loop-dependent and -independent manner

Project description:This SuperSeries is composed of the SubSeries listed below.

2026-05-06 | GSE275003 | GEO

CTCF couples long-range loop extrusion and diffusion to mediate a diverse Igk repertoire

Project description:Dynamic genome folding is important for V(D)J recombination at the immunoglobulin kappa (Igk) locus, which recombines Jk and Vk gene segments across a 3.2 Mb region in both deletional and inversional orientations. Chromatin loop extrusion and diffusion are considered two key mechanisms underlying Igk folding, but how they coordinate remains unclear. Here we show that CTCF is a key regulator coupling loop extrusion and diffusion during Igk V-J rearrangement, promoting recombination in both orientations across long genomic distances. Mechanistically, the CTCF N-terminus promotes long-range loop extrusion that facilitates distal Vk usage by stabilizing cohesin against WAPL release, and also forms loop barriers enabling chromatin diffusion for inversional Vk joining. In CTCF N-terminal-deficient B cells, defects in inversional Vk joining are not restored by WAPL depletion but are instead largely rescued by a dCas9-blockade targeted to the Vk-Jk intergenic region, mimicking the CTCF barrier. Our findings thus highlight how CTCF coordinates distinct genome-folding mechanisms through its dual roles in cohesin stabilization and extrusion barrier formation to ensure the generation of a diverse Igk repertoire.

2025-11-18 | PXD070894 | Pride

Chd4 regulates intra-chromatin looping by concealing CTCF sites from B2 SINEs in mESCs

Project description:CTCF plays a critical role in maintaining the three-dimensional (3D) chromatin organization, which is important for gene regulation, as it allows distal regulatory elements to come into proximity with one another. However, the detailed mechanism responsible for establishing and maintaining the recruitment of CTCF remains elusive. Here, we use in situ Hi-C to show that the ATP-dependent chromatin remodeler, Chd4, regulates intra-chromatin looping by controlling chromatin accessibility to conceal aberrant CTCF-binding sites in mouse embryonic stem cells (mESCs). These aberrant CTCF-binding sites are embedded in B2 SINEs and are localized within the interior of chromatin loops. In the absence of Chd4, the aberrant CTCF-binding sites become accessible and improper CTCF recruitment occurs, resulting in disorganization of the 3D chromatin architecture and subsequent disruption of enhancer-promoter interactions and the transcription of the corresponding genes. These results indicate that Chd4 regulates adequate transcription of mESCs by securing the proper 3D chromatin organization.

2022-05-10 | GSE172392 | GEO

CTCF couples long-range loop extrusion and diffusional mechanism to mediate a diverse Igk repertoire

Project description:Dynamic genome folding plays a crucial role in cellular functions, including V(D)J recombination at the immunoglobulin kappa (Igκ) locus for antibody generation. This process involves frequent recombination between Jκ and Vκ gene segments over a 3.2 Mb region in both deletional and inversional orientations. While loop extrusion and diffusion are thought to facilitate Igκ recombination, their cooperative mechanisms remain unclear. Our study demonstrates CTCF as a key regulator coupling loop extrusion and diffusion to enhance Vκ recombination in both orientations across large genomic distances. We show that CTCF's N-terminus promotes long-range loop extrusion important for distal Vκ usage by stabilizing cohesin against Wapl release. Furthermore, CTCF's loop barrier function is essential for inversional Vκ usage via enabling diffusion. In CTCF N-terminus mutants, defects in inversional Vκ joining were not corrected by Wapl depletion alone but improved with targeted dCas9 blockade mimicking the CTCF barrier. These findings reveal that CTCF regulates immune diversity via diverse mechanisms and underscore its versatility in gene regulation.

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