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Effect of hypoxia on the Represser Element-1 Silencing Transcription factor (REST) in Human

ABSTRACT: Effect of hypoxia on the Represser Element-1 Silencing Transcription factor (REST) in Human

PROVIDER: PRJEB6351 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR507055.fastq.gz	Fastqsanger.gz
	ERR507056.fastq.gz	Fastqsanger.gz
	ERR507057.fastq.gz	Fastqsanger.gz
	ERR507058.fastq.gz	Fastqsanger.gz
	ERR507059.fastq.gz	Fastqsanger.gz

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Effect of hypoxia on the Represser Element-1 Silencing Transcription factor (REST) in Human

Project description:The Represser Element-1 Silencing Transcription factor (REST) was knocked-down in HEK293 cells using RNA intereference in cells exposed to 21% or 1% oxygen for 24 hours, the effects on transcript expression (poly(A)+ RNA)) were analyzed using genome wide sequencing (RNAseq).

2016-08-17 | E-MTAB-2580 | biostudies-arrayexpress

Neuronal differentiation requires BRAT1 complex to remove REST from chromatin

Project description:Repressor element-1 silencing transcription factor (REST) is required for mature neurons formation. REST dysregulation underlies a key mechanism of neurodegeneration associated with neurological disorders. However, the mechanisms leading to alterations of REST-mediated silencing of key neurogenesis genes are not known. Here we show that BRAT1, a gene linked to neurodegenerative diseases, is required for activation of REST-responsive genes during neuronal-differentiation. We find that INTS11 and INTS9 subunits of Integrator complex interact with BRAT1 as a distinct trimeric complex to activate critical neuronal genes during differentiation. BRAT1 depletion results in persistence of REST residence on critical neuronal genes disrupting the differentiation of NT2 cells into astrocytes and neural cells. We identified BRAT1 and INTS11 co-occupying the promoter region of these genes and pinpoint a role for BRAT1 in recruiting INTS11 to their promoters. Disease-causing mutations in BRAT1 diminish its association with INTS11/INTS9, linking the manifestation of disease phenotypes with a defect in transcriptional activation of key neuronal genes by BRAT1/INTS11/INTS9 complex.

2025-05-06 | PXD050622 | Pride

REST-interactome - Interactomic analysis of REST/NRSF and implications of its functional links with the transcription suppressor TRIM28 during neuronal differentiation

Project description:Namgyu Lee has participated in the experimental part of this project and she is a co-first author of the under-going manuscript. RE-1 silencing transcription factor (REST) is a transcriptional repressor with a role in regulating gene expression through binding to repressor element 1. We identified REST/NRSF-interacting proteins by proteomics-based analyses using the complementary mass spectrometry approach. Our interactome revealed 204 REST-interacting proteins. Among those proteins, nuclear proteins were mostly enriched reflecting nuclear localization of REST. The interaction networks of interactome indicated biological processes associated with mRNA processing, chromatin organization and transcription. Interactions of ALYREF, HnRNP M, HnRNP Q, NPM1, NCL, PARP1, HDAC5, TRIM28 and HMGA1 with REST were confirmed by co-immunoprecipitation. Using public microarray dataset, a highly significant overlaps were observed in differentially expressed transcripts following knockdown of REST and interacting proteins such as HDAC5, HMGA1 and TRIM28, suggesting that the REST might cross-talk with those transcription regulators to regulate transcription of shared target genes. Our interactomic study of REST implies novel cross-talks with transcription regulators by its associations with interacting proteins.

2018-10-25 | PXD003210 | Pride

Transcriptional analysis of Rest/Nrsf silencing in N18 neuroblastoma cell line

Project description:The vertebrate-specific transcription factor RE-1 silencing transcription factor or neuron-restrictive silencer factor (REST/NRSF) was first described as a negative regulator restricting expression of neuronal genes to neurons in a variety of genetic contexts. However, REST/NRSF has a more general role in the regulation of gene expression that involves chromatin remodelling via a SWI/SNF complex. We identified a 677 gene repertoire of potential REST/NRSF-dependent genes taking advantage of Rest/Nrsf gene silencing in a mouse cell line. Using Ka/Ks analysis, we found that REST/NRSF protein, REST/NRSF interactors and the products of REST/NRSF-dependent genes display significantly higher rates of protein evolution in primates than in rodents. The McDonald-Kreitman test indicated positive selection for human REST/NRSF and nuclear RNA-binding proteins encoded by REST/NRSFdependent genes. In these proteins, we demonstrated sites under positive selection within the primate’s clade. Importantly, the REST/NRSF-dependent gene repertoire is statistically enriched in genes disrupted in neuropsychiatric diseases such as schizophrenia. In addition, we found that Smarca2 (Brm), Smarcd3 (Baf60c), Smarce1 (Baf57), Hdac1, RcoR1, and Mecp2, which are part of the REST/NRSFSWI/SNF chromatin remodelling complex, are transcriptionally regulated by REST/NRSF. Changing their gene dosage in vitro induced abnormal dendritic and dendritic spine phenotypes that were previously observed in rodent models of neuropsychiatric diseases. Altogether, these results suggest that genes encoding proteins of the REST/NRSF-SWI/SNF pathway display primate-specific accelerated evolution. It may be hypothesized that the subset of genes involved in this pathway, which display a primate evolutionary signature in specific sites, may represent a novel gene candidate repertoire for neuropsychiatric diseases.

2010-06-06 | GSE14326 | GEO

Epigenomic conservation of transposable element silencing

Project description:Epigenomic conservation of transposable element silencing

| PRJNA379439 | ENA

E-MTAB-2580

Project description:Effect of hypoxia on the Represser Element-1 Silencing Transcription factor (REST) in Human

2025-01-23 | E-MTAB-2580 | ExpressionAtlas

Mechanism of REST/NRSF Regulation of Clustered Protocadherin Alpha Genes

Project description:Repressor element-1 silencing transcription factor (REST) or neuron-restrictive silencer factor (NRSF) is a zinc-finger (ZF) containing transcriptional repressor that recognizes thousands of neuron-restrictive silencer elements (NRSEs) in mammalian genomes. How REST/NRSF regulates gene expression remains incompletely understood. Here, we investigate the binding pattern and regulation mechanism of REST/NRSF in the clustered protocadherin (PCDH) genes. We find that REST/NRSF directionally forms base-specific interactions with NRSEs via tandem ZFs in an anti-parallel manner but with striking conformational changes. In addition, REST/NRSF recruitment to the HS5-1 enhancer leads to the decrease of long-range enhancer-promoter interactions and downregulation of the clustered PCDH alpha genes. Thus, REST/NRSF represses PCDH alpha gene expression through directional binding to a repertoire of NRSEs within the distal enhancer and variable target genes.

2021-04-14 | GSE150254 | GEO

Transcription profiling of human U251 cells treated with hypoxia inducible factor HIF-1I siRNA or a polyamide targeted against the hypoxia response element (HRE) after induction of hypoxia

Project description:Transcription mediated by hypoxia inducible factor (HIF-1) contributes to tumor angiogenesis and metastasis but is also involved in the activation of cell-death pathways and normal physiological processes. Given the complexity of HIF-1 signaling it could be advantageous to target a subset of HIF-1 effectors rather than the entire pathway. We compared the genome-wide effects of three molecules that each interfere with the HIF-1-DNA interaction: a polyamide targeted to the hypoxia response element (HRE), siRNA targeted to HIF-1Î±, and echinomycin, a DNA binding natural product with a similar but less specific sequence preference to the polyamide. The polyamide affects a subset of hypoxia-induced genes that are consistent with the binding site preferences of the polyamide. For comparison, siRNA targeted to HIF-1α and echinomycin each affect the expression of nearly every gene induced by hypoxia. Remarkably, the total number of genes affected by either polyamide or HIF-1α siRNA over a range of thresholds is comparable. The data shows how polyamides can be used to affect a subset of a pathway regulated by a transcription factor. In addition, this study offers a unique comparison of three complementary approaches towards exogenous control of endogenous gene expression. Experiment Overall Design: Hypoxia-mimetic DFO (deferoxamine)-stimulated U251 cells that were treated with polyamide 1, HIF-1α siRNA, and echinomycin were compared to control cells that were also DFO-stimulated. Cells not stimulated with DFO were also compared to the DFO-stimulated controls. Three biological replicates were included for each treatment/condition.

2008-06-15 | E-GEOD-7835 | biostudies-arrayexpress

Epigenomic conservation of transposable element silencing [RNA-seq]

Project description:Epigenomic conservation of transposable element silencing [RNA-seq]

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Epigenomic conservation of transposable element silencing [ChIP-seq]

Project description:Epigenomic conservation of transposable element silencing [ChIP-seq]

| PRJNA379444 | ENA