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Analysis of three-dimensional enhancer network regulated by CTCF in CD4+ T cells [ChIP-seq]

ABSTRACT: Purpose: We aim to analyze genome-wide changes in RNA expression, histone modifications, chromatin structure, and 3D genome organization in CD4+ T cells following CTCF depletion. Conclusions: CTCF controls gene expression via 3D enhancer network in CD4+ T cells

ORGANISM(S): Mus musculus

PROVIDER: GSE243710 | GEO | 2026/01/12

REPOSITORIES: GEO

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Analysis of three-dimensional enhancer network regulated by CTCF in CD4+ T cells [HiChIP]

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Analysis of three-dimensional enhancer network regulated by CTCF in CD4+ T cells

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CTCF controls three-dimensional enhancer network underlying the inflammatory response of bone marrow-derived dendritic cells.

Project description:Dendritic cells are antigen-presenting cells orchestrating innate and adaptive immunity. The crucial role of transcription factors and histone modifications in the transcriptional regulation of dendritic cells has been extensively studied. However, it is not been well understood whether and how three-dimensional chromatin folding controls gene expression in dendritic cells. Here we demonstrate that activation of bone marrow-derived dendritic cells induces extensive reprogramming of chromatin looping as well as enhancer activity, both of which are implicated in the dynamic changes in gene expression. Interestingly, depletion of CTCF attenuates GM-CSF-mediated JAK2/STAT5 signaling, resulting in defective NF-κB activation. Moreover, CTCF is necessary for establishing NF-κB-dependent chromatin interactions and maximal expression of pro-inflammatory cytokines, which prime Th1 and Th17 cell differentiation. Collectively, our study provides mechanistic insights into how three-dimensional enhancer networks control gene expression during bone marrow-derived dendritic cells activation, and offers an integrative view of the complex activities of CTCF in the inflammatory response of bone marrow-derived dendritic cells.

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Role of the cellular factor CTCF in the regulation of Bovine Leukemia Virus latency and three-dimensional chromatin organization [4C-seq]

Project description:Bovine Leukemia Virus (BLV)-induced tumoral development is a multifactorial phenomenon which remains incompletely understood. Here, we highlight the critical role of the cellular CCCTC-binding factor (CTCF) both in the regulation of BLV transcriptional activities and in the deregulation of the three-dimensional (3D) chromatin architecture surrounding the BLV integration site. We demonstrated the in vivo recruitment of CTCF to three conserved CTCF binding motifs along the BLV provirus. Next, we showed the localization of CTCF to transitions in the histone modifications profile along BLV genome as well as its implication in the repression the 5’Long Terminal Repeat (LTR) promoter activity, thereby contributing to viral latency, while favoring the 3’LTR promoter activity. Finally, we demonstrated that BLV integration deregulated host cellular 3D chromatin organization through the formation of viral/host chromatin loops. Altogether, our results highlight CTCF as a new critical effector of BLV transcriptional regulation and BLV-induced physiopathology.

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ZNF143 deletion alters enhancer/promoter looping and CTCF/cohesin geometry [4C]

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