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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]

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

PROVIDER: PRJNA739197 | ENA |

REPOSITORIES: ENA

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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.

2022-02-18 | GSE178483 | GEO

CTCF binding polarity determines chromatin looping [4C]

Project description:CCCTC-binding factor (CTCF) is an architectural protein involved in the three-dimensional organization of chromatin. In this study, we systematically assayed the 3D genomic contact profiles of hundreds of CTCF binding sites in multiple tissues with high-resolution 4C-seq. We find both developmentally stable and dynamic chromatin loops. As recently reported, our data also suggest that chromatin loops preferentially form between CTCF binding sites oriented in a convergent manner. To directly test this, we used CRISPR-Cas9 genome editing to delete core CTCF binding sites in three loci, including the CTCF site in the Sox2 super-enhancer. In all instances, CTCF and cohesin recruitment were lost, and chromatin loops with distal CTCF sites were disrupted or destabilized. Re-insertion of oppositely oriented CTCF recognition sequences restored CTCF and cohesin recruitment, but did not re-establish chromatin loops. We conclude that CTCF binding polarity plays a functional role in the formation of higher order chromatin structure. 4C-seq was performed on a large number of viewpoints in E14 embryonic stem cells, neural precursor cells and primary fetal liver cells

2015-10-29 | E-GEOD-72539 | biostudies-arrayexpress

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

2022-02-18 | GSE178482 | GEO

CTCF binding polarity determines chromatin looping [4C]

2015-10-29 | GSE72539 | GEO

Role of the cellular factor CTCF in the regulation of Bovine Leukemia Virus latency and three-dimensional chromatin organization

Project description:Role of the cellular factor CTCF in the regulation of Bovine Leukemia Virus latency and three-dimensional chromatin organization

| PRJNA739194 | ENA

Three-dimensional analysis of genome organization in CTCF-WT and CTCF-KO dendritic cells

Project description:Three-dimensional analysis of genome organization in CTCF-WT and CTCF-KO dendritic cells

| PRJNA771097 | ENA

Three-dimensional analysis of genome organization in CTCF-WT and CTCF-KO dendritic cells (HiC)

Project description:Three-dimensional analysis of genome organization in CTCF-WT and CTCF-KO dendritic cells (HiC)

| PRJNA771092 | ENA

Three-dimensional analysis of genome organization in CTCF-WT and CTCF-KO dendritic cells (HiChIP)

Project description:Three-dimensional analysis of genome organization in CTCF-WT and CTCF-KO dendritic cells (HiChIP)

| PRJNA771099 | ENA

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

Project description:Role of the cellular factor CTCF in the regulation of Bovine Leukemia Virus latency and three-dimensional chromatin organization [ChIP-seq]

| PRJNA739198 | ENA

Multiple long-range cis interactions generate CTCF insulator-dependent viral chromatin domains in quiescent HSV-1 genomes

Project description:In cellular genomes, CTCF insulators impact transcription over small distances in a one-dimensional manner and over much longer distances in a three-dimensional manner by maintaining chromatin loops. We have previously shown that the latent HSV-1 genome contains CTCF insulators that function to regulate lytic transcription of adjacent genes in a one-dimensional manner. Here, we test the hypothesis that HSV-1 CTCF insulators nucleate chromatin loops to regulate the expression of distance separated gene regions through three-dimensional organization of viral genomes. We used 4C-seq methods to identify multiple long-range cis interactions in HSV-1 genomes that generate viral chromatin domains, including those nucleated by the viral CTCF insulator CTRL2. Deletion of the CTRL2 insulator disrupted these viral chromatin domains. Loop-nucleating interactions were quantitated with a novel approach (UMI-4C-seq) that utilizes unique molecular identifiers to label and count chromatin interactions associated with specific viewpoint primers. Cis-interaction peaks across four different viewpoints were quantified. Viral genomes lacking CTRL2 displayed more cis-interaction peaks and wider ranges of interaction lengths compared to wt virus, suggesting altered chromatin organization. Furthermore, differential looping analysis showed viral genomes lacking CTRL2 displayed a more transcriptionally permissive chromatin environment. Thus, the CTRL2 insulator functions as a critical regulator of long-range chromatin interactions and its deletion reshapes the viral chromatin landscape, leading to a more accessible and dynamic regulatory environment that may influence HSV-1 transcriptional programs and latency-associated chromatin states.

2025-07-03 | GSE301274 | GEO

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