Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mus musculus

ABSTRACT: Striatal genes regulated by super-enhancers and displaying low paused RNAPII are preferentially down-regulated in Huntington’s disease [RNA-seq]

PROVIDER: PRJNA255649 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR1519960.fastq.gz	Fastqsanger.gz
	SRR1519961.fastq.gz	Fastqsanger.gz
	SRR1519962.fastq.gz	Fastqsanger.gz
	SRR1519958.fastq.gz	Fastqsanger.gz
	SRR1519959.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 5

Similar Datasets

Mus musculus

Project description:Striatal genes regulated by super-enhancers and displaying low paused RNAPII are preferentially down-regulated in Huntington’s disease [ChIP-seq]

| PRJNA255650 | ENA

Striatal genes regulated by super-enhancers and displaying low paused RNAPII are preferentially down-regulated in Huntington's disease

Project description:Striatal genes regulated by super-enhancers and displaying low paused RNAPII are preferentially down-regulated in Huntington's disease

| PRJNA255648 | ENA

Striatal genes regulated by super-enhancers and displaying low paused RNAPII are preferentially down-regulated in Huntington’s disease [ChIP-seq]

Project description:Huntington neurodegenerative disease (HD) is associated with extensive down-regulation of neuronal genes. We show preferential down-regulation of super-enhancer-regulated neuronal function genes in the striatum of HD mice. Striatal super-enhancers display extensive H3K27 acetylation within gene bodies and drive transcription characterized by low levels of paused RNAPII. Down-regulation of gene expression is associated with diminished H3K27 acetylation and RNAPII recruitment. Striatal super-enhancers are enriched in binding motifs for Gata transcription factors, such as Gata2 regulating striatal identity genes. Thus, enhancer topography and transcription dynamics are major parameters determining the propensity of a gene to be deregulated in a neurodegenerative disease. Examination of H3k27ac and RNA pol II in Striatum by deep sequencing

2015-04-01 | E-GEOD-59570 | biostudies-arrayexpress

Striatal genes regulated by super-enhancers and displaying low paused RNAPII are preferentially down-regulated in Huntington’s disease [RNA-seq]

Project description:Huntington neurodegenerative disease (HD) is associated with extensive down-regulation of neuronal genes. We show preferential down-regulation of super-enhancer-regulated neuronal function genes in the striatum of HD mice. Striatal super-enhancers display extensive H3K27 acetylation within gene bodies and drive transcription characterized by low levels of paused RNAPII. Down-regulation of gene expression is associated with diminished H3K27 acetylation and RNAPII recruitment. Striatal super-enhancers are enriched in binding motifs for Gata transcription factors, such as Gata2 regulating striatal identity genes. Thus, enhancer topography and transcription dynamics are major parameters determining the propensity of a gene to be deregulated in a neurodegenerative disease. RNA profiles in Striatum of WT and R6/1 mice by deep sequencing using Illumina HiSeq 2000.

2015-04-01 | E-GEOD-59571 | biostudies-arrayexpress

Striatal genes regulated by super-enhancers and displaying low paused RNAPII are preferentially down-regulated in Huntington’s disease [ChIP-seq]

2015-04-01 | GSE59570 | GEO

Striatal genes regulated by super-enhancers and displaying low paused RNAPII are preferentially down-regulated in Huntington’s disease [RNA-seq]

2015-04-01 | GSE59571 | GEO

The Paf1 complex positively regulates enhancer activity in mouse embryonic stem cells

Project description:The RNA polymerase II (RNAPII) associated factor 1 complex (Paf1C) plays critical roles in modulating the release of paused RNAPII into productive elongation. However, regulation of Paf1C-mediated promoter-proximal pausing is complex and context dependent. In fact, in cancer cell lines opposing models of Paf1Cs’ role in RNAPII pause-release control have been proposed. Here we show that the Paf1C positively regulates RNAPII pause-release at both protein-coding genes and at enhancers in mouse embryonic stem cells (mESC). Our analyses reveal extensive Paf1C binding at mESC enhancers, in particular at super enhancers. Importantly, Paf1C occupancy correlates with the strength of enhancer activity. Depletion of Paf1C attenuates the expression of genes regulated by targeted enhancers and affects RNAPII Ser2 phosphorylation at the binding sites, suggesting that mESC self-renewal depends on Paf1C-mediated positive regulation of pluripotency enhancers.

2020-12-25 | GSE149999 | GEO

Widespread transcriptional pausing and elongation control at enhancers

Project description:Regulation by gene-distal enhancers is critical for cell-type and condition-specific patterns of gene expression. Thus, to understand the fundamental basis of gene activity in a given cell type or tissue, we must be able to identify the precise locations of enhancers, and to functionally characterize their behaviors. Herein, we demonstrate that transcription is nearly universal feature of enhancers in Drosophila and mammalian cells, and that nascent RNA-sequencing strategies are optimal for identification of both enhancers and super-enhancers. We dissect the mechanisms governing enhancer transcription and discover remarkable similarities with transcription at protein-coding genes. We show that RNA polymerase II (RNAPII) undergoes regulated pausing and release at enhancers. However, as compared to mRNA genes, RNAPII at enhancers is less stable and more prone to early termination. Further, we find that the level of histone H3 Lysine 4 (H3K4) methylation at enhancers corresponds to transcriptional activity, such that highly-active enhancers display H3K4 tri-methylation rather than H3K4 mono-methylation considered a hallmark of enhancers. Finally, our work provides insights into the unique characteristics of super-enhancers, which stimulate high-level gene expression through rapid pause release; interestingly, this property renders associated genes resistant to loss of factors that stabilize paused RNAPII.

2018-03-09 | GSE85191 | GEO

Targeting super-enhancer induced gene expression using novel BRD4 inhibitor OTX015 in preclinical models of MYCN-amplified neuroblastoma

Project description:Bromodomain-containing protein 4 (BRD4) functions as an epigenetic reader and binds to so-called super-enhancer regions of driving oncogenes such as MYC in cancer. We investigated the possibility to target super-enhancer regulated genes in neuroblastoma and in MYCN amplified disease in particular. We used OTX015, the first small-molecule BRD4 inhibitor to enter clinical phase I/II trials in adults, to test the feasibility to specifically target super-enhancer regulated gene-expression in neuroblastoma. BRD4 inhibition lead to significant transcriptional down-regulation of genes that were associated with super-enhancers, supporting the notion that BRD4 preferentially acts at these chromatin sites. BRD4 inhibition not only attenuated MYCN transcription but most significantly affected MYCN-regulated transcriptional programs.

2016-07-03 | E-MTAB-3672 | biostudies-arrayexpress

mNET-seq on COMPASS-degron cells

Project description:We measured the the dwell time of existed paused RNAPII at the promoter by mammalian native elongating transcript sequencing (mNET-seq). We found a median RNAPII half-life of 5.3 min at protein-coding genes in DMSO pre-treated control mESCs, whereas the RNAPII half-life at these genes significantly slowdown to 8.96 min when pre-treated with Auxin in the DPY30-mAID degron cell. The data suggested that loss H3K4me3 directly slows down the release of paused RNAPII throughout genes.

2023-01-20 | GSE181686 | GEO

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