Biochemically distinct states of cohesin mediate formation of loop and TAD domains
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE182500 | GEO | 2022/07/24
REPOSITORIES: GEO
Similar Datasets
Project description:The human genome folds to create thousands of intervals, called “contact domains,” that exhibit enhanced contact frequency within themselves. “Loop domains” form because of tethering between two loci – almost always bound by CTCF and cohesin – lying on the same chromosome. “Compartment domains” form when genomic intervals with similar histone marks co-segregate. Here, we explore the effects of degrading cohesin. All loop domains are eliminated, but neither compartment domains nor histone marks are affected. Loss of loop domains does not lead to widespread ectopic gene activation, but does affect a significant minority of active genes. In particular, cohesin loss causes superenhancers to co-localize, forming hundreds of links within and across chromosomes, and affecting the regulation of nearby genes. We then restore cohesin and monitor the re-formation of each loop. Although re-formation rates vary greatly, many megabase-sized loops recovered in under an hour, consistent with a model where loop extrusion is rapid.
2017-10-05 | GSE104333 | GEO
Project description:Cohesin loss eliminates all loop domains
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Project description:The human genome folds to create thousands of intervals, called “contact domains,” that exhibit enhanced contact frequency within themselves. “Loop domains” form because of tethering between two loci – almost always bound by CTCF and cohesin – lying on the same chromosome. “Compartment domains” form when genomic intervals with similar histone marks co-segregate. Here, we explore the effects of degrading cohesin. All loop domains are eliminated, but neither compartment domains nor histone marks are affected. Loss of loop domains does not lead to widespread ectopic gene activation, but does affect a significant minority of active genes. In particular, cohesin loss causes superenhancers to co-localize, forming hundreds of links within and across chromosomes, and affecting the regulation of nearby genes. We then restore cohesin and monitor the re-formation of each loop. Although re-formation rates vary greatly, many megabase-sized loops recovered in under an hour, consistent with a model where loop extrusion is rapid.
2017-11-15 | GSE106886 | GEO
Project description:The human genome folds to create thousands of intervals, called “contact domains,” that exhibit enhanced contact frequency within themselves. “Loop domains” form because of tethering between two loci – almost always bound by CTCF and cohesin – lying on the same chromosome. “Compartment domains” form when genomic intervals with similar histone marks co-segregate. Here, we explore the effects of degrading cohesin. All loop domains are eliminated, but neither compartment domains nor histone marks are affected. Loss of loop domains does not lead to widespread ectopic gene activation, but does affect a significant minority of active genes. In particular, cohesin loss causes superenhancers to co-localize, forming hundreds of links within and across chromosomes, and affecting the regulation of nearby genes. We then restore cohesin and monitor the re-formation of each loop. Although re-formation rates vary greatly, many megabase-sized loops recovered in under an hour, consistent with a model where loop extrusion is rapid.
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Project description:Cohesin loss eliminates all loop domains [HiC]
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Project description:Cohesin loss eliminates all loop domains [ChIP-Seq]
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Project description:Cohesin loss eliminates all loop domains [PRO-Seq]
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Project description: Not available
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Project description:The organization of chromatin into higher-order structures is essential for chromosome segregation, the repair of DNA damage, and the regulation of gene expression. These structures are formed by the evolutionarily conserved SMC (structural maintenance of chromosomes) complexes. By analyzing synchronized populations of budding yeast with Micro-C, we observed that chromatin loops are formed genome-wide, and are dependent upon the SMC complex, cohesin. We correlated the loop signal with the position and intensity of cohesin binding to chromosomes in wild-type and cells depleted for the cohesin regulators Wpl1p and Pds5p. We generate a model to explain how the genomic distribution and frequency of loops are driven by cohesin residency on chromosomes. In this model a dynamic pool of cohesin with loop extrusion activity stops when encounters two regions occupied by stably bound cohesin, forming a loop. Different regions are occupied by cohesin in different cells, defining different patterns of chromatin loops.
2020-11-04 | GSE151553 | GEO
Project description:The organization of chromatin into higher-order structures is essential for chromosome segregation, the repair of DNA damage, and the regulation of gene expression. These structures are formed by the evolutionarily conserved SMC (structural maintenance of chromosomes) complexes. By analyzing synchronized populations of budding yeast with Micro-C, we observed that chromatin loops are formed genome-wide, and are dependent upon the SMC complex, cohesin. We correlated the loop signal with the position and intensity of cohesin binding to chromosomes in wild-type and cells depleted for the cohesin regulators Wpl1p and Pds5p. We generate a model to explain how the genomic distribution and frequency of loops are driven by cohesin residency on chromosomes. In this model a dynamic pool of cohesin with loop extrusion activity stops when encounters two regions occupied by stably bound cohesin, forming a loop. Different regions are occupied by cohesin in different cells, defining different patterns of chromatin loops.
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