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A cohesin cancer mutation reveals a role for the hinge domain in genome organization and gene expression [Hi-C]

ABSTRACT: A cohesin cancer mutation reveals a role for the hinge domain in genome organization and gene expression [Hi-C]

PROVIDER: PRJNA643261 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12121510_1.fastq.gz	Fastqsanger.gz
	SRR12121510_2.fastq.gz	Fastqsanger.gz
	SRR12121511_1.fastq.gz	Fastqsanger.gz
	SRR12121511_2.fastq.gz	Fastqsanger.gz
	SRR12121512_1.fastq.gz	Fastqsanger.gz

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A cohesin cancer mutation reveals a role for the hinge domain in genome organization and gene expression [Hi-C]

Project description:Purpose: Chromatin loop formation and maintenance is regulated by the cohesin complex. Here, we investigate whether a cancer mutation to a cohesin complex subunit, SMC1A-R586W, alters genome architecture. Method: Genome wide chromatin looping patterns were assessed via Hi-C in both wildtype and CRISPR-Cas9 genome edited SMC1A-R586W mouse embryonic stem cells (mESCs).

2021-02-23 | GSE153574 | GEO

A cohesin cancer mutation reveals a role for the hinge domain in genome organization and gene expression

Project description:A cohesin cancer mutation reveals a role for the hinge domain in genome organization and gene expression

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Cohesin is a key determinant of interphase chromosome domain architecture (HiC)

Project description:To ensure proper gene regulation within constrained nuclear space, chromosomes facilitate access to transcribed regions, while compactly packaging all other information. Recent studies revealed that chromosomes are organized into megabase-scale domains that demarcate active and inactive genetic elements, suggesting that compartmentalization is important for genome function. Here we show that very specific long-range interactions are anchored by cohesin/CTCF sites, but not cohesin-only or CTCF-only sites, to form a hierarchy of chromosomal loops. These loops demarcate topological domains and form intricate internal structures within them. Post-mitotic nuclei deficient for functional cohesin exhibit global architectural changes associated with loss of cohesin/CTCF contacts and relaxation of topological domains. Transcriptional analysis shows that this cohesin-dependent perturbation of domain organization leads to widespread gene deregulation of both cohesin-bound and non-bound genes. Our data thereby support a role for cohesin in the global organization of domain structure and suggest that domains function to stabilize the transcriptional programs within them. Hi-C, ChIP-Seq and RNA-Seq experiments were conducted in mouse neural stem cells and mouse astrocytes

2013-12-11 | E-GEOD-49017 | biostudies-arrayexpress

Cohesin is a key determinant of interphase chromosome domain architecture (ChIP-seq)

2013-12-11 | E-GEOD-48938 | biostudies-arrayexpress

Cohesin is a key determinant of interphase chromosome domain architecture (RNA-seq)

2013-12-11 | E-GEOD-48965 | biostudies-arrayexpress

A cohesin cancer mutation reveals a role for the hinge domain in genome organization and gene expression [RNA-seq]

Project description:A cohesin cancer mutation reveals a role for the hinge domain in genome organization and gene expression [RNA-seq]

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A cohesin cancer mutation reveals a role for the hinge domain in genome organization and gene expression [ChIP-seq]

Project description:A cohesin cancer mutation reveals a role for the hinge domain in genome organization and gene expression [ChIP-seq]

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Evidence that Loading of Cohesin Onto Chromosomes Involves Opening of Its SMC Hinge

Project description:Cohesin is a multisubunit complex that mediates sister-chromatid cohesion. Its Smc1 and Smc3 subunits possess ABC-like ATPases at one end of 50 nm long coiled coils. At the other ends are pseudosymmetrical hinge domains that interact to create V-shaped Smc1/Smc3 heterodimers. N- and C-terminal domains within cohesin's kleisin subunit Scc1 bind to Smc3 and Smc1 ATPase heads respectively, thereby creating a huge tripartite ring. It has been suggested that cohesin associates with chromosomes by trapping DNA within its ring. Opening of the ring due to cleavage of Scc1 by separase destroys sister-chromatid cohesion and triggers anaphase. We show that cohesin's hinges are not merely dimerization domains. They are essential for cohesin's association with chromosomes, which is blocked by artificially holding hinge domains together but not by preventing Scc1's dissociation from SMC ATPase heads. Our results suggest that entry of DNA into cohesin's ring requires transient dissociation of Smc1 and Smc3 hinge domains. Keywords: Cohesin loading, Scc1, Smc1, Smc3, Hinge opening, ChIP-chip

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Comparative Hi-C reveals that CTCF underlies evolution of chromosomal domain architecture.

Project description:Topological domains are key architectural building blocks of chromosomes in complex genomes. Their functional importance and evolutionary dynamics are however not well defined. Here we performed comparative Hi-C in liver cells from four mammalian species, and characterized the conservation and divergence of chromosomal contact insulation and the resulting domain architectures within distantly related genomes. We show that the modular organization of chromosomes is robustly conserved in syntenic regions. This overall conservation is compatible with conservation of the binding landscape of the insulator protein CTCF. Specifically, conserved CTCF sites are co-localized with cohesin, enriched at strong topological domain borders and bind to DNA motifs with orientations that define the directionality of CTCF’s long-range interactions. Interestingly, CTCF binding sites which are divergent between species are strongly correlated with divergence of internal domain structure. This divergence is likely driven by local CTCF binding sequence changes, demonstrating how genome evolution can be linked directly with a continuous flux of local chromosome conformation changes. Conversely, we provide evidence that large-scale domains are harder to break and that they are reorganized during genome evolution as intact modules. Hi-C and 4C-seq experiments were conducted in primary liver cells obtained from mouse, rabbit, macaque and dog

2015-02-26 | E-GEOD-65126 | biostudies-arrayexpress

The cohesin ring uses its hinge to organize DNA using non-topological as well as topological mechanisms

Project description:As predicted by the notion that sister chromatid cohesion is mediated by entrapment of sister DNAs inside cohesin rings, there is a perfect correlation between co-entrapment of circular minichromosomes and sister chromatid cohesion. In most cells where cohesin loads onto chromosomes but fails to form cohesion, loading is accompanied by entrapment of individual DNAs. However, cohesin with a hinge whose positively charged lumen has been neutralized not only loads onto and translocates along chromatin but also organizes it into chromatid-like threads, despite largely failing to entrap DNAs inside its ring. Thus, cohesin engages chromatin in both a non-topological and a topological manner. Further, mutation of three highly conserved lysines within the Smc1 hinge abolishes all loading without affecting cohesin’s initial recruitment to centromers or its ability to hydrolyze ATP. We suggest that loading and translocation are mediated by conformational changes in cohesin’s hinge driven by cycles of ATP hydrolysis.

2018-04-23 | GSE105005 | GEO

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