Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Super-enhancer switching in early mammalian development involves eRNA mediated SWI/SNF recruitment

ABSTRACT: Super-enhancer switching in early mammalian development involves eRNA mediated SWI/SNF recruitment

PROVIDER: PRJNA992193 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR25098974.fastq.gz	Fastqsanger.gz
	SRR25098975.fastq.gz	Fastqsanger.gz
	SRR25098976.fastq.gz	Fastqsanger.gz
	SRR25098977.fastq.gz	Fastqsanger.gz
	SRR25098978.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 56

Similar Datasets

Super-enhancer switching in early mammalian development involves eRNA mediated SWI/SNF recruitment [CUT-RUN]

Project description:The RNA transcribed from enhancer regions, referred to as eRNA, has been suggested to directly activate transcription by helping to recruit transcription factors and co-activators. Although there have been specific examples of eRNA functioning in this way, it is not clear how general this may be. We find the AT-hook of SWI/SNF alone binds preferentially RNA and as part of the esBAF complexes associates with eRNA transcribed from intronic and intergenic regions. SWI/SNF is globally recruited in cis by eRNA to cell-type specific enhancers at two distinct stages in early mammalian development and not at promoters or enhancers that are shared between the two stages. SWI/SNF recruited by eRNA facilitates recruitment and/or activation of MLL3/4, p300/CBP and Mediator co-activators to stage-specific super-enhancers that in the primed embryonic stage activate cell lineage priming related genes. We find a strong connection between ATP-dependent chromatin remodeling and eRNA in cell identity and super-enhancer activation.

2023-08-25 | GSE207788 | GEO

Super-enhancer switching in early mammalian development involves eRNA mediated SWI/SNF recruitment [RIP-seq]

Project description:The RNA transcribed from enhancer regions, referred to as eRNA, has been suggested to directly activate transcription by helping to recruit transcription factors and co-activators. Although there have been specific examples of eRNA functioning in this way, it is not clear how general this may be. We find the AT-hook of SWI/SNF alone binds preferentially RNA and as part of the esBAF complexes likely associates with eRNA that are transcribed from intronic and intergenic regions. SWI/SNF is globally recruited in cis by eRNA to cell-type specific enhancers at two distinct stages in early mammalian development and not at promoters or enhancers that are shared between the two stages. SWI/SNF recruited by eRNA facilitates recruitment and/or activation of MLL3/4, p300/CBP and Mediator co-activators to stage-specific super-enhancers that in the primed embryonic stage activate cell lineage priming related genes. We find a strong connection between ATP-dependent chromatin remodeling and eRNA in cell identity and super-enhancer activation.

2023-07-10 | GSE236261 | GEO

Super-enhancer switching in early mammalian development involves eRNA mediated SWI/SNF recruitment [RNAPII_inhibitor CUT&RUN]

Project description:The RNA transcribed from enhancer regions, referred to as eRNA, has been suggested to directly activate transcription by helping to recruit transcription factors and co-activators. Although there have been specific examples of eRNA functioning in this way, it is not clear how general this may be. We find the AT-hook of SWI/SNF alone binds preferentially RNA and as part of the esBAF complexes likely associates with eRNA that are transcribed from intronic and intergenic regions. SWI/SNF is globally recruited in cis by eRNA to cell-type specific enhancers at two distinct stages in early mammalian development and not at promoters or enhancers that are shared between the two stages. SWI/SNF recruited by eRNA facilitates recruitment and/or activation of MLL3/4, p300/CBP and Mediator co-activators to stage-specific super-enhancers that in the primed embryonic stage activate cell lineage priming related genes. We find a strong connection between ATP-dependent chromatin remodeling and eRNA in cell identity and super-enhancer activation.

2023-07-10 | GSE236752 | GEO

Super-enhancer switching in early mammalian development involves eRNA mediated SWI/SNF recruitment [CUT-RUN]

Project description:Super-enhancer switching in early mammalian development involves eRNA mediated SWI/SNF recruitment [CUT-RUN]

| PRJNA857069 | ENA

Super-enhancer switching in early mammalian development involves eRNA mediated SWI/SNF recruitment [RIP-seq]

Project description:Super-enhancer switching in early mammalian development involves eRNA mediated SWI/SNF recruitment [RIP-seq]

| PRJNA989588 | ENA

Super-enhancer switching in early mammalian development involves eRNA mediated SWI/SNF recruitment [RNAPII_inhibitor CUT&RUN]

Project description:Super-enhancer switching in early mammalian development involves eRNA mediated SWI/SNF recruitment [RNAPII_inhibitor CUT&RUN]

| PRJNA992192 | ENA

Super-enhancer switching in early mammalian development involves eRNA mediated SWI/SNF recruitment

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

2023-07-08 | GSE236753 | GEO

siRNA Knockdown of SWI/SNF complex proteins in prostate cancer cell lines

Project description:Here we performed transcriptional profiling of the prostate cancer cell lines LNCaP and 22Rv1 comparing non-targeting siRNA treatment versus siRNAs targeting SWI/SNF complex proteins (SMARCA2, SMARCA4, and SMARCB1). Goal was to determine the effect of SWI/SNF knockdown on gene expression in prostate cancer. Two-condition experiment: non-targeting siRNA versus SWI/SNF-siRNA treated cells. Three SWI/SNF proteins were targeted: SMARCA2, SMARCA4, and SMARB1. Biological replicates: 1 control replicate, 2 treatment replicates per SWI/SNF protein. Technical replicates: 1 replicate per SWI/SNF protein. Cell lines: 22Rv1 and LNCaP.

2013-07-20 | E-GEOD-40384 | biostudies-arrayexpress

Genome-wide profile of the SWI/SNF chromatin remodeling complex

Project description:A systems understanding of nuclear organization and events is critical for determining how cells divide, differentiate and respond to stimuli and for identifying the causes of diseases. Chromatin remodeling complexes such as SWI/SNF have been implicated in a wide variety of cellular processes including gene expression, nuclear organization, centromere function and chromosomal stability, and mutations in SWI/SNF components have been linked to several types of cancer. To better understand the biological processes in which chromatin remodeling proteins participate we globally mapped binding regions for several components of the SWI/SNF complex throughout the human genome using ChIP-Seq. SWI/SNF components were found to lie near regulatory elements integral to transcription (e.g. 5M-bM-^@M-^Y ends, RNA Polymerases II and III and enhancers) as well as regions critical for chromosome organization (e.g. CTCF, lamins and DNA replication origins). To further elucidate the association of SWI/SNF subunits with each other as well as with other nuclear proteins we also analyzed SWI/SNF immunoprecipitated complexes by mass spectrometry. Individual SWI/SNF factors are associated with their own family members as well as with cellular constituents such as nuclear matrix proteins, key transcription factors and centromere components implying a ubiquitous role in gene regulation and nuclear function. We find an overrepresentation of both SWI/SNF-associated regions and proteins in cell cycle and chromosome organization. Taken together the results from our ChIP and immunoprecipitation experiments suggest that SWI/SNF facilitates gene regulation and genome function more broadly and through a greater diversity of interactions than previously appreciated. ChIP-Seq analysis of the SWI/SNF subunits Ini1, Brg1, BAF155 and BAF170 in HeLa S3 cells

2011-01-10 | E-GEOD-24397 | biostudies-arrayexpress

A SWI/SNF nucleosome remodeling complex acts in non-coding RNA-mediated transcriptional silencing

Project description:RNA-mediated transcriptional silencing prevents deleterious effects of transposon activity and controls the expression of protein-coding genes. It involves long non-coding RNAs (lncRNAs)1, which in Arabidopsis thaliana are produced by a specialized RNA Polymerase V (Pol V)2. lncRNAs guide Argonaute-siRNA complexes to specific genomic loci and mediate the establishment of DNA methylation3,4. The mechanism by which lncRNAs affect chromatin structure and mRNA production remains mostly unknown. Here we identify the SWI/SNF nucleosome remodeling complex as a component of the RNA-mediated transcriptional silencing pathway. We found that SWI3, an essential subunit of the SWI/SNF complex, physically interacts with a lncRNA-binding IDN2 protein5,6. RNA-mediated DNA methylation and transcriptional silencing was compromised in the swi3 mutant. Moreover, targets of SWI/SNF significantly overlapped with genes controlled by Pol V, which shows that the physical interaction reflects a functional relationship. We further found that non-coding transcription by Pol V affects nucleosome positioning on silenced regions. We propose that lncRNAs mediate transcriptional silencing by guiding the SWI/SNF complex and establishing positioned nucleosomes on specific genomic loci. We further propose that guiding ATP-dependent chromatin remodeling complexes may be a more general function of lncRNAs. RNA-seq of 3 samples (Col-0, nrpe1 [a mutant defective in the largest subunit of Pol V and unable to produce lncRNA], swi3b, idn2) with 3 biological replicates.

2012-12-01 | E-GEOD-38400 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data