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Capture Hi-C in (EV and ZFP661-3HA OE) mESCs and E16.5 mouse forebrains

ABSTRACT: Capture Hi-C in (EV and ZFP661-3HA OE) mESCs and E16.5 mouse forebrains

PROVIDER: PRJNA968173 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24461537_1.fastq.gz	Fastqsanger.gz
	SRR24461537_2.fastq.gz	Fastqsanger.gz
	SRR24461538_1.fastq.gz	Fastqsanger.gz
	SRR24461538_2.fastq.gz	Fastqsanger.gz
	SRR24461539_1.fastq.gz	Fastqsanger.gz

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Capture Hi-C in (EV and ZFP661-3HA OE) mESCs and E16.5 mouse forebrains

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 impacts of ZFP661 on the permeability of CTCF barriers to chromatin interactions. To achieve this, we generated high-resolution Hi-C maps using empty vector (EV) control and ZFP661-3HA overexpressing (OE) mESCs. Our findings demonstrate that ZFP661 suppresses the trapping of cohesin at the CTCF barriers and modulates their permeability.

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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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ChIP-seq data in mESCs show ZFP661 suppresses cohesin binding at CTCF barriers

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:In this assay, we aimed to investigate whether ZFP661 co-binds target regions with CTCF. To achieve this, we performed ChIP-reChIP-seq in ZFP661-3HA overexpressing (OE) mESCs, where the 1st ChIP utilized anti-HA antibody, and the 2nd ChIP involved the use of anti-IgG and anti-CTCF antibodies, respectively. Our results demonstrate that ZFP661 co-binds target regions with CTCF.

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