Cohesin-dependent and independent mechanisms support chromosomal contacts between promoters and enhancers (PCHiC)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA608019 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11142931_1.fastq.gz | Fastqsanger.gz | |||
| SRR11142931_2.fastq.gz | Fastqsanger.gz | |||
| SRR11142932_1.fastq.gz | Fastqsanger.gz | |||
| SRR11142932_2.fastq.gz | Fastqsanger.gz | |||
| SRR11142933_1.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:It is currently assumed that 3D chromosomal organisation plays a central role in transcriptional control. However, recent evidence shows that steady-state transcription of only a minority of genes is affected by depletion of architectural proteins such as cohesin and CTCF. Here, we have used Capture Hi-C to interrogate the dynamics of chromosomal contacts of all human gene promoters upon rapid architectural protein degradation. We show that promoter contacts lost in these conditions tend to be long-range, with at least one interaction partner localising in the vicinity of topologically associated domain (TAD) boundaries. In contrast, many shorter-range chromosomal contacts, particularly those that connect active promoters with each other and with active enhancers remain unaffected by cohesin and CTCF depletion. We demonstrate that the effects of cohesin depletion on nascent transcription can be explained by changes in the connectivity of their enhancers. Jointly, these results provide a mechanistic explanation to the limited, but consistent effects of cohesin and CTCF on steady-state transcription and point towards the existence of alternative enhancer-promoter pairing mechanisms that are independent of these proteins.
2020-07-13 | GSE145735 | GEO
Project description:Cohesin-dependent and independent mechanisms support chromosomal contacts between promoters and enhancers
| PRJNA608018 | ENA
Project description:It is currently assumed that 3D chromosomal organisation plays a central role in transcriptional control. However, recent evidence shows that steady-state transcription of only a minority of genes is affected by depletion of architectural proteins such as cohesin and CTCF. Here, we have used Capture Hi-C to interrogate the dynamics of chromosomal contacts of all human gene promoters upon rapid architectural protein degradation. We show that promoter contacts lost in these conditions tend to be long-range, with at least one interaction partner localising in the vicinity of topologically associated domain (TAD) boundaries. In contrast, many shorter-range chromosomal contacts, particularly those that connect active promoters with each other and with active enhancers remain unaffected by cohesin and CTCF depletion. We demonstrate that the effects of cohesin depletion on nascent transcription can be explained by changes in the connectivity of their enhancers. Jointly, these results provide a mechanistic explanation to the limited, but consistent effects of cohesin and CTCF on steady-state transcription and point towards the existence of alternative enhancer-promoter pairing mechanisms that are independent of these proteins.
2020-07-13 | GSE145734 | GEO
Project description:Cohesin-dependent and independent mechanisms support chromosomal contacts between promoters and enhancers (SLAM-Seq)
| PRJNA608020 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2020-07-13 | GSE145736 | GEO
Project description:It is currently assumed that 3D chromosomal organization plays a central role in transcriptional control. However, depletion of cohesin and CTCF affects the steady-state levels of only a minority of transcripts. Here, we use high-resolution Capture Hi-C to interrogate the dynamics of chromosomal contacts of all annotated human gene promoters upon degradation of cohesin and CTCF. We show that a majority of promoter-anchored contacts are lost in these conditions, but many contacts with distinct properties are maintained, and some new ones are gained. The rewiring of contacts between promoters and active enhancers upon cohesin degradation associates with rapid changes in target gene transcription as detected by SLAM sequencing (SLAM-seq). These results provide a mechanistic explanation for the limited, but consistent, effects of cohesin and CTCF depletion on steady-state transcription and suggest the existence of both cohesin-dependent and -independent mechanisms of enhancer-promoter pairing.
| S-EPMC7383238 | biostudies-literature
Project description:Mammalian chromosomes are partitioned into topologically associating domains (TADs) by the loop-extrusion activity of cohesin that is blocked at specific DNA sites bound by CTCF. Chromosome structure inside TADs is highly variable in single cells, yet little is known about its temporal dynamics, how it influences the rates and durations of chromosomal contacts, and how it depends on CTCF and cohesin. To address these questions we combine two quantitative live-cell imaging strategies that minimize locus-specific confounding effects. We show that loop extrusion by cohesin globally reduces the mobility of the chromatin fiber in living cells, while also increasing the rates of formation and durations of contacts between sequences inside the same TAD. Quantitative analysis of high-resolution microscopy data reveals that contacts assemble and disassemble frequently in the course of the cell cycle, and become substantially more frequent and longer in the presence of convergent CTCF sites. Comparison with polymer modeling additionally reveals that cohesin-mediated CTCF loops last around 10 minutes on average. Our data support the notion that chromosome structure within TADs is highly dynamic and provide a quantitative framework for understanding the principles that link chromosome structure to biological function.
2022-02-27 | GSE197234 | GEO
Project description:Mammalian chromosomes are partitioned into topologically associating domains (TADs) by the loop-extrusion activity of cohesin that is blocked at specific DNA sites bound by CTCF. Chromosome structure inside TADs is highly variable in single cells, yet little is known about its temporal dynamics, how it influences the rates and durations of chromosomal contacts, and how it depends on CTCF and cohesin. To address these questions we combine two quantitative live-cell imaging strategies that minimize locus-specific confounding effects. We show that loop extrusion by cohesin globally reduces the mobility of the chromatin fiber in living cells, while also increasing the rates of formation and durations of contacts between sequences inside the same TAD. Quantitative analysis of high-resolution microscopy data reveals that contacts assemble and disassemble frequently in the course of the cell cycle, and become substantially more frequent and longer in the presence of convergent CTCF sites. Comparison with polymer modeling additionally reveals that cohesin-mediated CTCF loops last around 10 minutes on average. Our data support the notion that chromosome structure within TADs is highly dynamic and provide a quantitative framework for understanding the principles that link chromosome structure to biological function.
2022-02-27 | GSE197231 | GEO
Project description:Mammalian chromosomes are partitioned into topologically associating domains (TADs) by the loop-extrusion activity of cohesin that is blocked at specific DNA sites bound by CTCF. Chromosome structure inside TADs is highly variable in single cells, yet little is known about its temporal dynamics, how it influences the rates and durations of chromosomal contacts, and how it depends on CTCF and cohesin. To address these questions we combine two quantitative live-cell imaging strategies that minimize locus-specific confounding effects. We show that loop extrusion by cohesin globally reduces the mobility of the chromatin fiber in living cells, while also increasing the rates of formation and durations of contacts between sequences inside the same TAD. Quantitative analysis of high-resolution microscopy data reveals that contacts assemble and disassemble frequently in the course of the cell cycle, and become substantially more frequent and longer in the presence of convergent CTCF sites. Comparison with polymer modeling additionally reveals that cohesin-mediated CTCF loops last around 10 minutes on average. Our data support the notion that chromosome structure within TADs is highly dynamic and provide a quantitative framework for understanding the principles that link chromosome structure to biological function.
2022-02-27 | GSE197226 | GEO
Project description:Mammalian chromosomes are partitioned into topologically associating domains (TADs) by the loop-extrusion activity of cohesin that is blocked at specific DNA sites bound by CTCF. Chromosome structure inside TADs is highly variable in single cells, yet little is known about its temporal dynamics, how it influences the rates and durations of chromosomal contacts, and how it depends on CTCF and cohesin. To address these questions we combine two quantitative live-cell imaging strategies that minimize locus-specific confounding effects. We show that loop extrusion by cohesin globally reduces the mobility of the chromatin fiber in living cells, while also increasing the rates of formation and durations of contacts between sequences inside the same TAD. Quantitative analysis of high-resolution microscopy data reveals that contacts assemble and disassemble frequently in the course of the cell cycle, and become substantially more frequent and longer in the presence of convergent CTCF sites. Comparison with polymer modeling additionally reveals that cohesin-mediated CTCF loops last around 10 minutes on average. Our data support the notion that chromosome structure within TADs is highly dynamic and provide a quantitative framework for understanding the principles that link chromosome structure to biological function.
2022-02-27 | GSE197237 | GEO