Refine regulatory elements across the genome
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA627176 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11581666_1.fastq.gz | Fastqsanger.gz | |||
| SRR11581666_2.fastq.gz | Fastqsanger.gz | |||
| SRR11581667_1.fastq.gz | Fastqsanger.gz | |||
| SRR11581667_2.fastq.gz | Fastqsanger.gz | |||
| SRR11581668_1.fastq.gz | Fastqsanger.gz |
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Project description:We develop an experimental method termed as MAE-seq, to identify active enhancer across the genome. Enhancer loci are mapped precisely to 25 bp in different types of cells. In mouse embryonic stem cells, 19,514 active enhancers are identified including 49.25% known and 50.75% de novo ones. In human HEK293T cell , 3,0359 active enhancers are identified.
2023-04-20 | GSE149028 | GEO
Project description:Proper cell fate determination relies on precise spatial and temporal genome-wide cooperativities among regulatory elements (REs) and their targeted genes. However, the lengths of REs defined by different methods are varied, which indicates sequence redundancy contained and the context of the genome will be unintelligible. To figure this out, we developed a method termed as MAE-seq (Massive Active Enhancers by Sequencing) to experimentally identify functional REs at a 25-bp scale. In this study, more than 626,879 active enhancers are identified in mouse embryonic stem cells. Comparative analysis indicates most of histone modification datasets could be annotated by MAE-Seq loci. Additionally, 35.03% (219,623) are identified as de novo ones without any epigenetic modification. Validation results show that these 25-bp sequences could act as a functional unit, which shows identical or similar expression patterns as the previously defined larger elements. Additionally, we examined the functions of some novel elements that can up-regulate gene activities. By integrating with Hi-C data, over 55.64% novel elements may have distal association with different targeted genes. As an example, we find Cdh1 gene is interacting with one novel and two known REs in mESCs. And their biological effects are investigated via CRISPR-Cas9. It indicates these distal associations can coordinate Cdh1 gene expression and mESCs proliferation. Therefore, our study provides an experimental approach to refine the REs at 25-bp resolution and it will be a great improvement to unscramble the underlying genome context.
2023-01-06 | GSE193494 | GEO
Project description:In this study, we have applied ChIP-Seq to identify putative regulatory elements throughout the zebrafish genome. For this purpose we identified sequences within the zebrafish genome that associate with H3K4me1 and H3K4me3, which are epigenetic modifications known to be associated with active cis-regulatory elements in other species. Determination of H3K4me1- and H3K4me3-binding sites in the zebrafish genome.
2011-02-25 | E-GEOD-20600 | biostudies-arrayexpress
Project description:MAE-seq refines regulatory elements across the genome
| PRJNA796352 | ENA
Project description:In this study, we have applied ChIP-Seq to identify putative regulatory elements throughout the zebrafish genome. For this purpose we identified sequences within the zebrafish genome that associate with H3K4me1 and H3K4me3, which are epigenetic modifications known to be associated with active cis-regulatory elements in other species.
2011-02-25 | GSE20600 | GEO
Project description:Background Genomic variations contribute to the phenotypic diversity of individuals. A number of polymorphisms in protein-coding regions that alter drug efficacy or lead to adverse reactions have been characterized; however, noncoding regions that affect drug responses are largely overlooked, except for a limited number of well-studied enhancers. Results We conducted a quantitative assessment of cis-regulatory elements (CREs) based on transcription initiation profiling of mRNAs and noncoding RNAs, including enhancer RNAs, by using CAGE (Cap Analysis of Gene Expression). Candidate CREs identified in a hepatocellular carcinoma HepG2 cell line with stable expression of drug-responsive transcription factor pregnane X receptor (PXR) were further narrowed down by integrating data of PXR-binding sites in human primary hepatocytes and genome-wide association studies. We found more than 100-fold enrichments of the candidates to genetically associated loci with circulating levels of bilirubin and vitamin D, which implicated a link to adverse reactions of PXR ligands. We uncovered novel enhancers of UGT1A1 and TSKU through CRISPR/Cas9 knockout experiments. We identified alleles altering regulatory activities of UGT1A1 and CYP24A1enhancers by using luciferase reporter assay. Furthermore, our siRNA experiments revealed an unexpected impact of TSKU on the expression of vitamin D-metabolizing enzymes. Conclusions Our transcriptome-based assessment of CREs expanded the list of drug-inducible and PXR-mediated enhancers and super-enhancers. We identified regulatory alleles that alter drug-induced gene expressions, and discovered a novel molecular cascade associated with an adverse reaction. Our results contribute a precise understanding of the noncoding elements of the human genome underlying drug responses.
2025-04-17 | PXD060446 | Pride
Project description:Identifying transcriptional networks active during development has been hindered by the slow pace at which regulatory elements are identified, and by the difficulty in purifying cells from developing tissues. We used DNaseI-seq to identify functional regulatory elements in purified fetal preSertoli cells and uncovered thousands of preSertoli-specific DNaseI hypersensitive sites (DHSs) that are likely to activate or repress genes required for Sertoli cell development and function. To demonstrate their functional significance, we validated the preSertoli-specific enhancer activity of a DHS located 50 kb upstream of the Wt1 gene. This genome-wide data will guide many future studies into gene-regulatory mechanisms that operate in the fetal gonad and may lead to the identification of non-coding mutations leading to DSDs. One biological replicate was analyzed for each of the seven mouse samples using DNase-seq.
2013-12-07 | E-GEOD-53076 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below. Large genome mapping consortia and thousands of genome-wide association studies have identified non-protein coding elements in the genome as a having a central role in tissue development, cell-type specification, response to environmental or pharmacologic signals, and susceptibility to most common diseases. However, decoding the function of the millions of putative regulatory elements discovered in these studies remains a primary challenge. New CRISPR/Cas9-based epigenome editing technologies have enabled the precise perturbation of the activity of specific regulatory elements. Here we describe CRISPR/Cas9-based Epigenomic Regulatory Element Screening (CERES) for high-throughput screening of regulatory element activity within the native genomic context. We perform both loss- and gain-of-function screens with complementary epigenome editing tools to identify known and unknown regulatory elements of medically relevant genes in human cells. The high-throughput functional annotation of putative regulatory elements by CERES constitutes a new platform for screening biological mechanisms that cannot be perturbed by traditional methods.
2017-03-23 | GSE96876 | GEO
Project description:Transcription factors (TFs) bind specific sequences in promoter-proximal and distal DNA elements in order to regulate gene transcription. RNA is transcribed from both promoter-proximal and distal DNA elements, and some DNA-binding TFs have also been shown to bind RNA. These obsevations led us to postulate that RNA transcribed from regulatory elements contributes to stable TF occupancy at these regulatory elements. We show here that the ubiquitously expressed TF YY1 binds to both proximal and distal regulatory elements and to the RNA species associated with these elements near active genes in embryonic stem cells. Inhibition of transcription from these elements reduces YY1 occupancy. In contrast, tethering of RNA species near YY1 DNA binding sites enhances YY1 occupancy. We propose that RNA acts as trap to maintain certain TFs at active enhancer and promoter-proximal regulatory elements. Thus, transcriptional control generally involves a positive feedback loop, where YY1 and other TFs stimulate local transcription, and newly transcribed nascent RNA reinforces local TF occupancy. This model helps explain why TFs occupy only the small fraction of their consensus motifs in the mammalian genome where transcription is detected. Affinity purification (ChIP-Seq) for YY1 in mouse embryonic stem cells treated with transcription-affecting compounds
2015-05-28 | E-GEOD-68195 | biostudies-arrayexpress
Project description:Large genome mapping consortia and thousands of genome-wide association studies have identified non-protein coding elements in the genome as a having a central role in tissue development, cell-type specification, response to environmental or pharmacologic signals, and susceptibility to most common diseases. However, decoding the function of the millions of putative regulatory elements discovered in these studies remains a primary challenge. New CRISPR/Cas9-based epigenome editing technologies have enabled the precise perturbation of the activity of specific regulatory elements. Here we describe CRISPR/Cas9-based Epigenomic Regulatory Element Screening (CERES) for high-throughput screening of regulatory element activity within the native genomic context. We perform both loss- and gain-of-function screens with complementary epigenome editing tools to identify known and unknown regulatory elements of medically relevant genes in human cells. The high-throughput functional annotation of putative regulatory elements by CERES constitutes a new platform for screening biological mechanisms that cannot be perturbed by traditional methods.
2017-03-23 | GSE96874 | GEO