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Mus musculus

ABSTRACT: Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [HiC-seq]

PROVIDER: PRJNA379860 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5362833_1.fastq.gz	Fastqsanger.gz
	SRR5362833_2.fastq.gz	Fastqsanger.gz
	SRR5362834_1.fastq.gz	Fastqsanger.gz
	SRR5362834_2.fastq.gz	Fastqsanger.gz
	SRR5362836_1.fastq.gz	Fastqsanger.gz

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Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure

Project description:Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure

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Loss of CTCF reveals basic properties of post-mitotic epigenomes and induces heart failure [HiC-seq]

Project description:Understanding the principles of endogenous chromatin structure has key implications for epigenetic therapy. To determine the mechanisms of genome structure-function in post-mitotic cells, genome-wide chromatin conformation capture was performed in cardiac myocytes, a non-dividing, differentiated cell responsible for cardiac contraction. Cardiac-specific CTCF knockout mice demonstrated that loss of CTCF had minimal effect on topologically associating domains; however, it selectively altered boundary strength and A/B compartmentalization, with gene expression changes mimicking those in heart failure. Loss of CTCF (or subjecting wild-type mice to clinically relevant pressure overload stress) remodeled long-range chromatin looping to alter 3D proximity of enhancers and disease causing genes. Depletion of CTCF was sufficient to induce heart failure in mice and human heart failure patients receiving mechanical unloading to attenuate disease progression show increased CTCF expression. These findings establish CTCF in the maintenance of chromatin looping and identify global chromatin remodeling as a causative factor in heart failure.

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Genome-wide mapping of CTCF binding in asynchronous and mitotic cells

Project description:CCCTC-binding factor (CTCF), a conserved and essential regulator of genome architecture bearing a unique complement of 11 zinc fingers (ZFs), has been reported to remain associated with chromatin throughout mitosis and has thus been proposed to act as a bookmark to ensure rapid reestablishment of chromatin structure after cell division. However, little is known about how CTCF is regulated during mitosis. Using a phospho-specific antibody, we found that phosphorylation of CTCF threonine 431, contained within an atypical ZF linker unique to vertebrate CTCF, is highly enriched in mitotic cells and that this phosphorylated form of CTCF is preferentially localized to mitotic chromosomes. We show that T431 mutations abolish the association of CTCF with mitotic chromatin, arguing that T431 phosphorylation is necessary for CTCF mitotic retention. Furthermore, mutation of the CTCF paralog BORIS to accommodate phosphorylation at the residue corresponding to CTCF T431 induces mitotic retention of BORIS. Our data support previous work demonstrating mitotic retention of CTCF and provide new insight into how CTCF remains associated with chromatin during mitosis. Furthermore, our results indicate that phosphorylation of ZF linkers is not exclusively associated with dissociation of ZF-containing proteins from DNA during mitosis.

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