RB is a cell cycle-regulated repressor of cohesin-dependent loop formation
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB70877 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12342562.fastq.gz | Fastqsanger.gz | |||
| ERR12342563.fastq.gz | Fastqsanger.gz | |||
| ERR12342564.fastq.gz | Fastqsanger.gz | |||
| ERR12342565.fastq.gz | Fastqsanger.gz | |||
| ERR12342566.fastq.gz | Fastqsanger.gz |
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Project description:Chromatin organization and cell cycle are tightly intertwined in eukaryotes, but the underlying mechanisms remain unclear. We investigated how the retinoblastoma protein (RB), a key cell cycle regulator, influences chromatin architecture. Chromosome conformation capture assays reveal that RB loss increases the number and size of cohesin-dependent loops and strengthens topologically associating domains (TADs). RB shows extensive colocalization with cohesin in the human genome, and it impacts cohesin’s distribution on chromatin. Active RB evicted cohesin from RB-bound TAD boundaries, repressed insulator activity, and enhanced the expression of non-E2F target genes that are important for cell adhesion. We conclude that RB has a central role in the interplay between cell cycle and chromatin organization. This role safeguards chromatin architecture and controls transcription.
2024-11-01 | E-MTAB-13566 | biostudies-arrayexpress
Project description: Not available
| S-BSST1221 | biostudies-other
Project description:Cohesin structures the genome through the formation of chromatin loops and by holding together the sister chromatids. The acetylation of cohesin’s SMC3 subunit is a dynamic process that involves the acetyltransferase ESCO1 and deacetylase HDAC8. Here we show that this cohesin acetylation cycle controls the 3D genome. ESCO1 restricts the length of chromatin loops and architectural stripes, while HDAC8 promotes the extension of such loops and stripes. This role in controlling loop length turns out to be distinct from the canonical role of cohesin acetylation that protects against WAPL-mediated DNA release. We reveal that acetylation rather controls cohesin’s interaction with PDS5A to restrict chromatin loop length. Our data supports a model in which this PDS5A-bound state acts as a brake that enables the pausing and restart of loop enlargement. The cohesin acetylation cycle hereby provides punctuation in the process of genome folding.
2022-03-14 | PXD032185 | Pride
Project description:The ring-shaped cohesin complex topologically entraps two DNAs to establish sister chromatid cohesion. Cohesin also shapes the interphase chromatin landscape, with wide-ranging implications for gene regulation, which cohesin is thought to achieve by actively extruding DNA loops without topologically entrapping DNA. The ‘loop extrusion’ model find motivation from in vitro observations - whether this process indeed underlies chromatin loop formation in vivo remains untested. Here, using the budding yeast S. cerevisiae, we generate cohesin variants that have lost their ability to extrude DNA loops but retain their ability to topologically entrap DNA. Analysis of these variants suggests that in vivo chromatin loops form independently of loop extrusion. Instead, we find that transcription promotes loop formation, likely by generating DNA substrates for topological loop capture. Transcription furthermore acts as an extrinsic motor that, by pushing cohesin along transcription units, extends chromatin loops and defines their ultimate positions. Our results necessitate a re-evaluation of the loop extrusion hypothesis and point to an alternative mechanism for cohesin-dependent chromatin organisation. Loop formation by DNA-DNA capture, akin to sister chromatid cohesion establishment at replication forks, unifies cohesin’s two roles in chromosome segregation and interphase genome organisation.
2024-08-04 | GSE248281 | GEO
Project description:The ring-shaped cohesin complex topologically entraps two DNAs to establish sister chromatid cohesion. Cohesin also shapes the interphase chromatin landscape, with wide-ranging implications for gene regulation, which cohesin is thought to achieve by actively extruding DNA loops without topologically entrapping DNA. The ‘loop extrusion’ model find motivation from in vitro observations - whether this process indeed underlies chromatin loop formation in vivo remains untested. Here, using the budding yeast S. cerevisiae, we generate cohesin variants that have lost their ability to extrude DNA loops but retain their ability to topologically entrap DNA. Analysis of these variants suggests that in vivo chromatin loops form independently of loop extrusion. Instead, we find that transcription promotes loop formation, likely by generating DNA substrates for topological loop capture. Transcription furthermore acts as an extrinsic motor that, by pushing cohesin along transcription units, extends chromatin loops and defines their ultimate positions. Our results necessitate a re-evaluation of the loop extrusion hypothesis and point to an alternative mechanism for cohesin-dependent chromatin organisation. Loop formation by DNA-DNA capture, akin to sister chromatid cohesion establishment at replication forks, unifies cohesin’s two roles in chromosome segregation and interphase genome organisation.
2024-08-04 | GSE248280 | GEO
Project description:Cohesin chromatin loop formation by an extrinsic motor
| PRJNA1043156 | ENA
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 | GSE151416 | 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.
2020-11-04 | GSE151553 | GEO
Project description:Cohesin structures the genome through the formation of chromatin loops and by holding together the sister chromatids from S-phase until mitosis. The acetylation of cohesin’s SMC3 subunit is a dynamic process that involves the acetyltransferase ESCO1 and deacetylase HDAC8. Here we show that this cohesin acetylation cycle controls the 3D genome. ESCO1 restricts the length of chromatin loops and architectural stripes, while HDAC8 rather promotes the extension of such loops and stripes. This role in controlling loop length turns out to be distinct from the canonical role of cohesin acetylation that protects against WAPL-mediated DNA release. We reveal that acetylation rather controls cohesin’s interaction with PDS5A to restrict chromatin loop length. Our data supports a model in which this PDS5A-bound state acts as a brake that enables the pausing and restart of loop enlargement. The cohesin acetylation cycle hereby provides punctuation in the process of genome folding.
2022-03-14 | GSE150564 | GEO
Project description:Cohesin loss eliminates all loop domains
| PRJNA412386 | ENA