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Reduced chromatin accessibility correlates with resistance to Notch activation

ABSTRACT: Reduced chromatin accessibility correlates with resistance to Notch activation

PROVIDER: PRJNA638637 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11977412.fastq.gz	Fastqsanger.gz
	SRR11977413.fastq.gz	Fastqsanger.gz
	SRR11977414.fastq.gz	Fastqsanger.gz
	SRR11977415.fastq.gz	Fastqsanger.gz
	SRR11977416.fastq.gz	Fastqsanger.gz

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Reduced chromatin accessibility correlates with resistance to Notch activation

Project description:The Notch signalling pathway is a master regulator of cell fate transitions in development and disease. In the brain, Notch promotes neural stem cell (NSC) proliferation, regulates neuronal migration and maturation and can act as an oncogene or tumour suppressor. How NOTCH and its transcription factor RBPJ activate distinct gene regulatory networks in closely related cell types in vivo remains to be determined. Here we use Targeted DamID (TaDa), requiring only thousands of cells, to identify NOTCH and RBPJ binding in NSCs and their progeny in the mouse embryonic cerebral cortex in vivo. We find that NOTCH and RBPJ associate with a broad network of NSC genes. Repression of NSC-specific Notch target genes in intermediate progenitors and neurons correlates with decreased chromatin accessibility, suggesting that chromatin compaction may contribute to restricting NOTCH-mediated transactivation.

2022-01-07 | GSE152207 | GEO

Placental Inflammation Significantly Correlates with Reduced Risk for Retinopathy of Prematurity

Project description:Placental Inflammation Significantly Correlates with Reduced Risk for Retinopathy of Prematurity

| PRJNA901967 | ENA

Reduced polymerase pausing compensates for increased chromatin accessibility in the aging liver

Project description:Regulation of gene expression is linked to the organization of the genome. With age, chromatin alterations occur on all levels of genome organization, accompanied by changes in the gene expression profile. However, little is known about the changes on the level of transcriptional regulation. Here, we used a multi-omics approach and integrated ATAC-, RNA- and NET-seq to identify age-related changes in the chromatin landscape of murine liver and to investigate how these are linked to transcriptional regulation. We provide the first systematic inventory of the connection between aging, chromatin accessibility and transcriptional regulation in a whole tissue. Aging in murine liver is characterized by an increase in chromatin accessibility at promoter regions, but not in an increase of transcriptional output. Instead, aging is accompanied by a decrease of promoter-proximal pausing of RNA polymerase II (Pol II). We propose that these changes in transcriptional regulation are due to a reduced stability of the pausing complex and may represent a mechanism to compensate for the age-related increase in chromatin accessibility in order to prevent aberrant transcription.

2022-09-15 | PXD034564 | Pride

Notch induces transcription by stimulating release of paused RNA Pol II without increasing chromatin accessibility [TT-seq]

Project description:Notch proteins undergo ligand-induced proteolysis to release a nuclear effector that influences a wide range of cell fate decisions by regulating gene activity. However, despite years of study, how Notch induces the transcription of its target genes remains unclear. Here, we comprehensively examined the response to human Notch1 across a time course of activation, using genomic assays of nascent RNA and chromatin accessibility. These data revealed that Notch induces target gene transcription primarily by releasing paused RNA polymerase II (RNAPII), in contrast to prevailing models suggesting that Notch acts by promoting chromatin accessibility. Indeed, we found that open chromatin is established at Notch-responsive regulatory elements prior to Notch signaling, through SWI/SNF-mediated remodeling. Notch activation, however, elicited no further chromatin opening at these loci. Together, these studies reveal that the nuclear response to Notch signaling is dictated by the pre-existing chromatin state and RNAPII distribution at the time of signal activation.

2024-06-13 | GSE269116 | GEO

Notch induces transcription by stimulating release of paused RNA Pol II without increasing chromatin accessibility [ChIP-seq]

2024-06-13 | GSE269113 | GEO

Notch induces transcription by stimulating release of paused RNA Pol II without increasing chromatin accessibility [PRO-seq]

2024-06-13 | GSE269115 | GEO

Notch induces transcription by stimulating release of paused RNA Pol II without increasing chromatin accessibility [ATAC-seq]

2024-06-13 | GSE269112 | GEO

Changes in the chromatin accessibility landscape of mouse embryonic endocardial cells after Notch pathway manipulation

Project description:Analysis by ATAC-seq of the changes in chromatin accessibility in MEEC due to the activity of Notch ligands.

2023-12-08 | GSE223733 | GEO

Notch

Project description:Notch

| PRJNA988118 | ENA

Analysis of HUVEC secretome and histone N-terminal acetylation after Notch activation

Project description:Vasculature permeate our entire body and involved in homeostasis and progression of various disease. Endothelium is a backbone of cardiovascular system and endothelial disfunction is associated with most forms of cardiovascular disease from atherosclerosis to chronic heart failure. Decrease in shear stress, particularly due to disturbance of the blood flow by bends or vascular obstruction, lead to atherosclerosis and endothelial disfunction. Notch signaling may act as mechanosensor and assumed to be one of the central signal pathways associated with endothelial disfunction. Association of shear stress, Notch and endothelial dysfunction is well known, molecular mechanisms connected these factors still poorly understood. One might assume that long-term shear stress and dysregulation of Notch in endothelium cause changes in epigenomic profile. While epigenomic changes in shear stressed environment are known to be involved in endothelial disfunction, possible connection of Notch and epigenetic changes in endothelium has not yet been tested. Therefore, here we analyzed how activation of Notch signaling influence on histone code and secretome of endothelial cells in vitro. We found that activation of Notch increase level of N-acetylated forms of Histone 1: H1-0, H1-3, H1-4, H1-5, H1-10. These changes were also associated with changes in secretome profile of endothelium and might have broad biomedical significance in case of endothelial dysfunction.

2023-02-15 | PXD032978 | Pride

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