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High affinity enhancer promoter interactions can bypass strong CTCF/cohesin-mediated insulation contributing to phenotypic robustness [Capture Hi-C]

ABSTRACT: High affinity enhancer promoter interactions can bypass strong CTCF/cohesin-mediated insulation contributing to phenotypic robustness [Capture Hi-C]

PROVIDER: PRJNA786863 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17156044_1.fastq.gz	Fastqsanger.gz
	SRR17156044_2.fastq.gz	Fastqsanger.gz
	SRR17156045_1.fastq.gz	Fastqsanger.gz
	SRR17156045_2.fastq.gz	Fastqsanger.gz
	SRR17156046_1.fastq.gz	Fastqsanger.gz

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High affinity enhancer promoter interactions can bypass strong CTCF/cohesin-mediated insulation contributing to phenotypic robustness

Project description:High affinity enhancer promoter interactions can bypass strong CTCF/cohesin-mediated insulation contributing to phenotypic robustness

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High affinity enhancer promoter interactions can bypass strong CTCF/cohesin-mediated insulation contributing to phenotypic robustness [ChIP-seq]

Project description:High affinity enhancer promoter interactions can bypass strong CTCF/cohesin-mediated insulation contributing to phenotypic robustness [ChIP-seq]

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High affinity enhancer promoter interactions can bypass strong CTCF/cohesin-mediated insulation contributing to phenotypic robustness [ChIP-seq]

Project description:Transcriptional control by enhancers located at large genomic distances from their targets is a common and integral feature of gene regulation. To understand how tissue specific enhancer-promoter interactions arise and to assess their resilience to perturbation of chromatin architecture, we generated an allelic series of mouse mutants carrying modifications to the structure of the Sox2 locus. We show that in pre-implantation epiblast cells and in neuronal lineages, CTCF-mediated loops are neither required for the interaction of Sox2 with its long-distance enhancers nor for its expression. Sox2-enhancer interactions in these cells were also robust to the introduction of CTCF/cohesin-mediated loops of varying degrees of insulation. These loops led to reduced interactions and Sox2 expression but did not cause their full disruption and were compatible with implantation and neurogenesis. In contrast, Sox2 expression in the anterior foregut was highly susceptible to perturbation of local chromatin structure with mutant embryos failing to separate trachea from esophagus and dying perinatally. Thus, in addition to being locus-specific, the functional impact of nuclear organization on cell fate-decisions is also highly dependent on biological context. Our work highlights the need of studying nuclear organization mechanisms in vivo and suggests that high-affinity enhancer-promoter interactions can provide robustness to structural perturbations to ensure faithful phenotypic outcomes.

2022-01-17 | GSE190358 | GEO

High affinity enhancer promoter interactions can bypass strong CTCF/cohesin-mediated insulation contributing to phenotypic robustness [Capture Hi-C]

2021-12-30 | GSE190357 | GEO

High affinity enhancer promoter interactions can bypass strong CTCF/cohesin-mediated insulation contributing to phenotypic robustness

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

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FGF19 as a Surgical Factor Contributing to the Metabolic Effects of Gastric Bypass Surgery

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FGF19 as a Surgical Factor Contributing to the Metabolic Effects of Gastric Bypass Surgery

Project description:Gastric bypass surgery has proven to be the most effective treatment in controlling hyperglycemia in severely obese patients with diabetes. Here we show that FGF19, a gut hormone, is rapidly induced by bypass surgery in rodents and humans. Administration of FGF19 achieves remission of diabetes through mechanisms beyond weight loss in animal models of diabetes, supporting a role of FGF19 as part of hormonal changes that influence metabolism following surgery. Through an unbiased phenotypic screen in diabetic mice, we identified selective, safe and effective FGF19 analogues. Unexpectedly, FGF19 analogue failed to correct hyperglycemia in patients with type 2 diabetes. In contrast, administration of FGF19 analogue resulted in rapid, robust and sustained improvement in liver fat content and histology in patients with non-alcoholic steatohepatitis, faithfully replicating effect of the surgery. Thus, our work identifies a strategy of replacing gastric bypass surgery by equally effective, but less invasive, treatment for non-alcoholic steatohepatitis. We used microarrays to detail the global programme of gene expression affected by gastric bypass surgery in rats.

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