ChIP-seq data in WT and Zfp661 knockout E16.5 mouse forebrains
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE256449 | GEO | 2024/02/24
REPOSITORIES: GEO
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Project description:In this assay, we aimed to investigate the impact of ZFP661 on the expression diversity of clustered protocadherin genes (Pcdhs). To accomplish this, we conducted single-cell 5’ RNA-seq analysis on developing mouse forebrains at embryonic day 16.5 (E16.5). Our findings reveal that ZFP661 enhances the expression diversity of Pcdhs by balancing the usage of Pcdh isoforms.
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Project description:This assay aimed to investigate the regulatory role of ZFP661 in modulating the permeability of CTCF barriers. To achieve this, we generated Capture Hi-C maps on several regions bound by ZFP661 using E16.5 forebrains from wild-type (WT) and Zfp661 knockout (KO) mice, as well as empty vector (EV) control and ZFP661-3HA overexpressing (OE) mESCs. Our findings reveal that ZFP661 modulates the permeability of CTCF barriers, thereby balancing between the interactions that are trapped at the barriers and those passing over them.
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Project description:In this assay, we aimed to investigate the occupancy of ZFP661 in the mouse genome and its possible role in regulating the occupancies of CTCF and cohesin, which are two key factors in establishing 3D chromatin structures. To achieve this, we performed ChIP-seq in ZFP661-3HA endogenously tagged mESCs (for ZFP661), Zfp661 knockout (KO) mESCs (for CTCF and RAD21), and ZFP661-3HA overexpressing (OE) mESCs (for ZFP661, CTCF, RAD21, KAP1, and H3K9me3). Our results reveal that 1) ZFP661 binding peaks were co-occupied with those of CTCF; 2) ZFP661 binds exclusively inside the CTCF loop anchors; and 3) ZFP661 can suppress cohesin binding at CTCF barriers without altering CTCF binding.
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Project description:The architectural protein CTCF binds to mammalian insulators genome wide with directionality and recruits cohesin to mediate oriented long-distance chromatin loops. In many cases, CTCF-binding sites (CBSs) are associated with distal enhancers and target promoters. It is generally thought that CTCF binding results in spatial contacts between distal enhancers and target promoters leading to activation of specific promoters. However, how CTCF orchestrates higher-order chromatin organization to regulate gene expression is not fully understood. Here we used CRISPR DNA-fragment editing to investigate the roles of CTCF in chromatin organization of the clustered protocadherin (Pcdh) genes, which is an ideal model system with repertoires of CBSs in variable promoters and super-enhancers. We found that the CBSs at chromatin domain boundary and even single CBSs could determine the orientation of long-distance chromatin looping. In addition, deletion or inversion of large regions containing tandem CBS arrays in mice demonstrated asymmetric influences on chromatin looping between super-enhancers and target promoters. These genetic data have important implications on the assembly mechanisms of higher-order chromatin structures.
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