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

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

PROVIDER: PRJNA723291 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14286500_1.fastq.gz	Fastqsanger.gz
	SRR14286500_2.fastq.gz	Fastqsanger.gz
	SRR14286600_1.fastq.gz	Fastqsanger.gz
	SRR14286600_2.fastq.gz	Fastqsanger.gz
	SRR14286700_1.fastq.gz	Fastqsanger.gz

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

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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.

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

Project description:This SuperSeries is composed of the SubSeries listed below.

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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

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