Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Compatibility logic of human enhancer and promoter sequences

ABSTRACT: Compatibility logic of human enhancer and promoter sequences

PROVIDER: PRJNA764659 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR15970700_1.fastq.gz	Fastqsanger.gz
	SRR15970700_2.fastq.gz	Fastqsanger.gz
	SRR15970701_1.fastq.gz	Fastqsanger.gz
	SRR15970701_2.fastq.gz	Fastqsanger.gz
	SRR15970702_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 258

Similar Datasets

Compatibility logic of human enhancer and promoter sequences

Project description:We transfected K562 cells with a STARR-seq plasmid library of paired promoter and enhancer sequences to characterize activation and compatibility between promoters and enhancers.

2021-10-25 | GSE184426 | GEO

Systematic analysis of intrinsic enhancer-promoter compatibility in the mouse genome.

Project description:Gene expression is in part controlled by cis-regulatory elements (CREs) such as enhancers and repressive elements. Anecdotal evidence has indicated that a CRE and a promoter need to be biochemically compatible for promoter regulation to occur, but this compatibility has remained poorly characterised in mammalian cells. By systematic reporter assays of thousands of CRE – promoter pairs from three Mb-sized genomic regions in mouse cells, we found that CREs vary substantially in their promoter compatibility, with more than half showing significant selectivity. This selectivity does not correlate with looping interactions, suggesting that chromatin folding and compatibility are two orthogonal mechanisms of gene regulation.

2021-10-21 | GSE186265 | GEO

Systematic analysis of intrinsic enhancer-promoter compatibility in the mouse genome.

Project description:Systematic analysis of intrinsic enhancer-promoter compatibility in the mouse genome.

| PRJNA773091 | ENA

Complementary Alu sequences mediate enhancer-promoter selectivity

Project description:Complementary Alu sequences mediate enhancer-promoter selectivity

| PRJNA786348 | ENA

Complementary Alu sequences mediate enhancer-promoter selectivity

Project description:Enhancers determine spatiotemporal gene expression programs by engaging with long-range promoters. However, it remains unknown how enhancers find their cognate promoters. We recently developed a RIC-seq technology to identify enhancer-promoter connectivity using pairwise interacting enhancer RNAs and promoter-derived noncoding RNAs in HeLa cells. Here, we apply this technology to generate high-confidence enhancer-promoter RNA interaction (EPRI) maps in six additional cell lines. Using these maps, we discover that 37.9% of the enhancer-promoter RNA interaction sites are overlapped with Alu sequences. These pairwise interacting Alu and non-Alu RNA sequences tend to be complementary and potentially form duplexes. Knockout of Alu elements compromises enhancer-promoter looping, whereas Alu insertion or CRISPR-dCasRx-mediated Alu tethering to unregulated promoter RNAs can create new loops to homologous enhancers. Importantly, mapping 535,404 noncoding risk variants back to the EPRI maps enabled us to construct variant-to-function maps for interpreting their molecular functions, including 15,318 deletions or insertions in 11,677 Alu elements that affect 6,497 protein-coding genes. We further demonstrate that polymorphic Alu insertion at PTK2 enhancer can promote tumorigenesis. Our study uncovers a principle for determining enhancer-promoter pairing specificity and provides a framework to link noncoding risk variants to their molecular functions.

2023-05-11 | GSE190214 | GEO

Miswired enhancer logic drives translocation positive rhabdomyosarcoma

Project description:Core regularity transcription factors (CR TFs) define cell identity and lineage through an exquisitely precise and logical order during embryogenesis and development. These CR TFs regulated one another in three-dimensional space via distal enhancers that serve as logic gates embedded in their TF recognition sequences. Aberrant chromatin organization resulting in miswired circuitry of enhancer logic is a newly recognized feature in many cancers. Here, we report that PAX3-FOXO1 expression is driven by a translocated FOXO1 distal super enhancer (SE). ChIP-seq in tumors bearing rare PAX translocations implicate enhancer miswiring is a pervasive feature across all FP-RMS tumors. Therefore, our data reveal a mechanism of a translocated hijacked enhancer which disrupts the normal CR TF logic during skeletal muscle development (PAX3 to MYOD to MYOG), replacing it with an infinite loop logic that makes rhabdomyosarcoma cells unable to exit the undifferentiated proliferating stage.

2019-12-25 | GSE136799 | GEO

Multiplex enhancer-reporter assays uncover unsophisticated p53 enhancer logic

Project description:Multiplex enhancer-reporter assays uncover unsophisticated p53 enhancer logic

| PRJNA308235 | ENA

Miswired enhancer logic drives translocation positive rhabdomyosarcoma

Project description:Miswired enhancer logic drives translocation positive rhabdomyosarcoma

| PRJNA563682 | ENA

Enhancer Cis Elements Instruct Promoter-Enhancer Interaction, Promoter-Enhancer Insulation and Compartmental Segregation

Project description:Enhancer Cis Elements Instruct Promoter-Enhancer Interaction, Promoter-Enhancer Insulation and Compartmental Segregation

| PRJNA881254 | ENA

High-throughput functional comparison of promoter and enhancer activities

Project description:Promoters initiate RNA synthesis, and enhancers stimulate promoter activity. Whether promoter and enhancer activities are encoded distinctly in DNA sequences is unknown. We measured the enhancer and promoter activities of thousands of DNA fragments transduced into mouse neurons. We focused on genomic loci bound by the neuronal activity-regulated co-activator CREBBP, and we measured enhancer and promoter activities both before and after neuronal activation. We find that the same sequences typically encode both enhancer and promoter activities. However, gene promoters generate more promoter activity than distal enhancers, despite generating similar enhancer activity. Surprisingly, the greater promoter activity of gene promoters is not due to conventional core promoter elements or splicing signals. Instead, we find that particular transcription factor binding motifs are intrinsically biased toward the generation of promoter activity, while others are not. While the specific biases we observe may be dependent on experimental or cellular context, our results suggest that gene promoters are distinguished from distal enhancers by specific complements of transcriptional activators.

2016-05-23 | GSE77213 | 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