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Genetic Evidence for Asymmetric Blocking of Higher-Order Chromatin Structure by CTCF/Cohesin

ABSTRACT: Genetic Evidence for Asymmetric Blocking of Higher-Order Chromatin Structure by CTCF/Cohesin

PROVIDER: PRJNA560861 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9995530.fastq.gz	Fastqsanger.gz
	SRR9995540.fastq.gz	Fastqsanger.gz
	SRR9995550.fastq.gz	Fastqsanger.gz
	SRR9995560.fastq.gz	Fastqsanger.gz
	SRR9995531.fastq.gz	Fastqsanger.gz

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Genetic Evidence for Asymmetric Blocking of Higher-Order Chromatin Structure by CTCF/Cohesin

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.

2019-09-15 | GSE135967 | GEO

Genetic evidence for asymmetric blocking of higher-order chromatin structure by CTCF/cohesin.

Project description: Not available

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Wapl controls higher-order chromatin structure in interphase chromosomes (gene expression)

Project description:Mammalian genomes contain several billion base pairs of DNA which are packaged in chromatin fibers. At selected gene loci, cohesin complexes have been proposed to arrange chromatin fibers into higher-order structures, but it is poorly understood how cohesin performs this task, how important this function is for determining the structure of chromosomes, and how this process is regulated to allow changes in gene expression. Here we show that the cohesin release factor Wapl controls chromatin structure and gene regulation at numerous loci throughout the mouse genome. Conditional deletion of the Wapl gene leads to stable accumulation of cohesin on chromatin, chromatin compaction, altered gene expression, cell cycle delay, chromosome segregation defects and embryonic lethality. In Wapl deficient chromosomes, cohesin accumulates in an axial domain, similar to how condensins form a M-bM-^@M-^\scaffoldM-bM-^@M-^] in mitotic chromosomes. We propose that Wapl controls chromatin structure and gene regulation by determining the residence time with which cohesin binds to DNA. 4 biological replicates for each genotype (Wapl +/F; Wapl -/F) treated with/without 4-OHT =16 samples

2013-08-09 | E-GEOD-41460 | biostudies-arrayexpress

Wapl controls higher-order chromatin structure in interphase chromosomes (ChIP-Seq)

Project description:Mammalian genomes contain several billion base pairs of DNA which are packaged in chromatin fibers. At selected gene loci, cohesin complexes have been proposed to arrange chromatin fibers into higher-order structures, but it is poorly understood how cohesin performs this task, how important this function is for determining the structure of chromosomes, and how this process is regulated to allow changes in gene expression. Here we show that the cohesin release factor Wapl controls chromatin structure and gene regulation at numerous loci throughout the mouse genome. Conditional deletion of the Wapl gene leads to stable accumulation of cohesin on chromatin, chromatin compaction, altered gene expression, cell cycle delay, chromosome segregation defects and embryonic lethality. In Wapl deficient chromosomes, cohesin accumulates in an axial domain, similar to how condensins form a “scaffold” in mitotic chromosomes. We propose that Wapl controls chromatin structure and gene regulation by determining the residence time with which cohesin binds to DNA. ChIP-Seq using two different antibodies (CTCF, Smc3); one (CTCF) and two (Smc3) replicates; two different genotypes (Wapl +/delta, Wapl -/delta). The control sample is a single-replicate INPUT for each genotype.

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DNA methylation maintains integrity of higher order genome architecture

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Engineered CRISPR-Cas12a for higher-order combinatorial chromatin perturbations

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