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An alternative CTCF isoform antagonizes canonical CTCF occupancy and changes chromatin architecture to promote apoptosis

ABSTRACT: An alternative CTCF isoform antagonizes canonical CTCF occupancy and changes chromatin architecture to promote apoptosis

PROVIDER: PRJNA428981 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6453220_1.fastq.gz	Fastqsanger.gz
	SRR6453220_2.fastq.gz	Fastqsanger.gz
	SRR6453230_1.fastq.gz	Fastqsanger.gz
	SRR6453230_2.fastq.gz	Fastqsanger.gz
	SRR6453221_1.fastq.gz	Fastqsanger.gz

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An alternative CTCF isoform antagonizes canonical CTCF occupancy and changes chromatin architecture to promote apoptosis

Project description:CTCF plays key roles in gene regulation, chromatin insulation, imprinting, X chromosome inactivation and organizing the higher-order chromatin architecture of mammalian genomes. Previous studies have mainly focused on the roles of the canonical CTCF isoform. Here, we explore the functions of an alternatively spliced human CTCF isoform in which exons 3 and 4 are skipped, producing a shorter isoform (CTCF-s). Functionally, we find that CTCF-s competes with the genome binding of canonical CTCF and binds a similar DNA sequence. CTCF-s binding disrupts CTCF/cohesin binding, alters CTCF-mediated chromatin looping and promotes the activation of IFI6 that leads to apoptosis. This effect is caused by an abnormal long-range interaction at the IFI6 enhancer and promoter. Taken together, this study reveals a non-canonical function for CTCF-s that antagonizes the genomic binding of canonical CTCF and cohesin, and that modulates chromatin looping and causes apoptosis by stimulating IFI6 expression.

2019-01-12 | GSE108869 | GEO

An alternative CTCF isoform antagonizes canonical CTCF occupancy and changes chromatin architecture to promote apoptosis.

Project description: Not available

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CGGBP1 regulates chromatin barrier activity and CTCF occupancy at repeats

Project description:To study the role of CGGBP1 in regulation of CTCF occupancy, we performed CTCF ChIP-seq in HEK293T cells with three different levels of CGGBP1: (i) endogenous levels of CGGBP1 (ii) CGGBP1 knockdown, and (iii) CGGBP1 overexpression. Here, we show that CTCF binds to repeats as well as canonical CTCF-motifs and CGGBP1 determines the CTCF occupancy preference for repeats over canonical CTCF-motif. By combining CTCF ChIP-seq with histone modifications ChIP-seq (for H3K4me3, H3K9me3 and H3K27me3) under conditions of normal or CGGBP1 knockdown, we demonstrate that CTCF binding sites regulated by CGGBP1 correspond to chromatin barrier elements with profound effects on H3K9me3 distribution. In conclusion, these finding shows that CGGBP1 is a regulator of CTCF occupancy and serve as a regulator of barrier functions of CTCF-binding sites.

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CTCF/CP190 and ISWI dependent regulation of nucleosome occupancy [MNase-seq]

Project description:MNase-seq was performed in order to analyze changes in nucleosomal occupancy after depletion of CTCF/P190 and ISWI from Drosophila S2 cells MNase-seq from Drosophila S2 nuclei after CTCF/CP190 or ISWI-specific RNAi treatment

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CTCF occupancy in the mouse telencephalon and medial ganglionic eminence

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