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Activity-induced gene expression and long-range enhancer-promoter contacts in cohesin-deficient neurons (Ribo Tag)

ABSTRACT: Activity-induced gene expression and long-range enhancer-promoter contacts in cohesin-deficient neurons (Ribo Tag)

PROVIDER: PRJNA723296 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14286539_1.fastq.gz	Fastqsanger.gz
	SRR14286539_2.fastq.gz	Fastqsanger.gz
	SRR14286540_1.fastq.gz	Fastqsanger.gz
	SRR14286540_2.fastq.gz	Fastqsanger.gz
	SRR14286541_1.fastq.gz	Fastqsanger.gz

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Cohesin-dependent and independent mechanisms support chromosomal contacts between promoters and enhancers (PCHiC)

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

Activity-induced gene expression and long-range enhancer-promoter contacts in cohesin-deficient neurons

Project description:Activity-induced gene expression and long-range enhancer-promoter contacts in cohesin-deficient neurons

| PRJNA723291 | ENA

Cohesin-dependent and independent mechanisms support chromosomal contacts between promoters and enhancers (SLAM-Seq)

2020-07-13 | GSE145734 | GEO

Activity-induced gene expression and long-range enhancer-promoter contacts in cohesin-deficient neurons (NexCre)

Project description:Activity-induced gene expression and long-range enhancer-promoter contacts in cohesin-deficient neurons (NexCre)

| PRJNA723293 | ENA

Activity-induced gene expression and long-range enhancer-promoter contacts in cohesin-deficient neurons with BDNF

Project description:Activity-induced gene expression and long-range enhancer-promoter contacts in cohesin-deficient neurons with BDNF

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Ribo-tag translatome analysis from Split-Cre transgenic mice

Project description:We generated Split-Cre transgenic mice strains to target microglia or Lyve1+ macrophages in the brain. To obtain translatome from the each population, Split-Cre mice were crossed with Ribo-tag reporter mice, and translatome were acquired with anti-HA antibody immuno-percipitation.

2020-08-18 | GSE156368 | GEO

Activity-induced gene expression and long-range enhancer-promoter contacts in cohesin-deficient neurons (Ribo Tag)

Project description:RNA-seq of ribosome associated mRNA from Rad21lox/lox;NexCre/+;RiboTag+ and Rad21+/+;NexCre/+;RiboTag+ dissociated cortical neurons at Day In Vitro (DIV10)

2022-04-26 | GSE172428 | GEO

Long-range chromosome interactions mediated by cohesin shape circadian gene expression [4C]

Project description:Mammalian circadian rhythm is established by the negative feedback loops consisting of a set of clock genes, which lead to the circadian expression of thousands of downstream genes. As genome-wide transcription is organized under the high-order chromosome structure, it is unclear how circadian gene expression is influenced by chromosome structure. In this study, we focus on the function of chromatin structure proteins cohesin as well as CTCF (CCCTC-binding factor) in circadian rhythm. We analyzed the interactome of a Bmal1-bound enhancer upstream of a clock gene, Nr1d1, by 4C-seq and observed that cohesin binding sites are enriched in the interactome. Integrating circadian transcriptome data and cistrome data, we found that cohesin-CTCF co-binding sites tend to insulate the phases of circadian oscillating genes while cohesin-non-CTCF sites facilitate the interaction between circadian enhancer and promoter. A coarse-grained model integrating the long-range effect of cohesin and CTCF markedly improved our mechanistic understanding of circadian gene expression. This model is subsequently supported by our RNA-seq data from cohesin knockout cells. Cohesin is required at least in part for driving the circadian gene expression by facilitating the enhancer-promoter looping. Taken together, our study provided a novel insight into the relationship between circadian transcriptome and the high-order chromosome structure. 4C-seq of a Bmal1 enhancer in mouse liver

2016-04-04 | E-GEOD-68830 | biostudies-arrayexpress

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

Structure of the Cohesin Loader Scc2-Scc4 and its Binding to a Folded Cohesin

Project description:The functions of cohesin are central to genome integrity, chromosome organization, and transcription regulation through its prevention of premature sister-chromatid separation and the formation of DNA loops. The loading of cohesin onto chromatin depends on the Scc2-Scc4 complex, however, little is known about how it stimulates the cohesin loading activity. Here we determine the large “hook” structure of Scc2 responsible for catalyzing cohesin loading. We identify key Scc2 surfaces that are crucial for DNA binding and for cohesin loading in vivo. Using previously determined structures and modeling, we derive a pseudo-atomic structure of the full-length Scc2-Scc4 complex. Finally, our crosslinking and electron microscopy analyses reveal that Scc2-Scc4 utilizes its modular structure to make multiple contacts with a folded cohesin at an interface created by the cohesin head-hinge interaction.

2017-01-11 | PXD004692 | Pride

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