Widespread transcriptional pausing and elongation control at enhancers
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA336521 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4000120_1.fastq.gz | Fastqsanger.gz | |||
| SRR4000120_2.fastq.gz | Fastqsanger.gz | |||
| SRR4000130_1.fastq.gz | Fastqsanger.gz | |||
| SRR4000130_2.fastq.gz | Fastqsanger.gz | |||
| SRR4000140_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 123 |
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Project description:Widespread transcriptional pausing and elongation control at enhancers
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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.
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Project description:Regulation by gene-distal enhancers is critical for cell type-specific and condition-specific patterns of gene expression. Thus, to understand the basis of gene activity in a given cell type or tissue, we must identify the precise locations of enhancers and functionally characterize their behaviors. Here, we demonstrate that transcription is a nearly universal feature of enhancers in Drosophila and mammalian cells and that nascent RNA sequencing strategies are optimal for identification of both enhancers and superenhancers. We dissect the mechanisms governing enhancer transcription and discover remarkable similarities to transcription at protein-coding genes. We show that RNA polymerase II (RNAPII) undergoes regulated pausing and release at enhancers. However, as compared with mRNA genes, RNAPII at enhancers is less stable and more prone to early termination. Furthermore, we found that the level of histone H3 Lys4 (H3K4) methylation at enhancers corresponds to transcriptional activity such that highly active enhancers display H3K4 trimethylation rather than the H3K4 monomethylation considered a hallmark of enhancers. Finally, our work provides insights into the unique characteristics of superenhancers, which stimulate high-level gene expression through rapid pause release; interestingly, this property renders associated genes resistant to the loss of factors that stabilize paused RNAPII.
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Project description:Gene transcription occurs via a cycle of linked events including initiation, promoter proximal pausing and elongation of RNA polymerase II (Pol 2). A key question is how do transcriptional enhancers influence these events to control gene expression? Here we have used a new approach to quantify transcriptional initiation and pausing in-vivo, while simultaneously identifying transcription start sites (TSSs) and pause-sites (TPSs). When analysed in parallel with nascent RNA-seq, these data show that differential gene expression is achieved predominantly via changes in transcription initiation rather than Pol 2 pausing or elongation. Using genetically engineered mouse models deleted for specific enhancers we show that these elements control gene expression via Pol 2 recruitment and/or initiation rather than via promoter proximal pause release. Using genome-wide analysis we show that enhancers, in general, control gene expression at the stage of Pol 2 recruitment and initiation rather than via pausing.
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Project description:Gene transcription occurs via a cycle of linked events including initiation, promoter proximal pausing and elongation of RNA polymerase II (Pol 2). A key question is how do transcriptional enhancers influence these events to control gene expression? Here we have used a new approach to quantify transcriptional initiation and pausing in-vivo, while simultaneously identifying transcription start sites (TSSs) and pause-sites (TPSs). When analysed in parallel with nascent RNA-seq, these data show that differential gene expression is achieved predominantly via changes in transcription initiation rather than Pol 2 pausing or elongation. Using genetically engineered mouse models deleted for specific enhancers we show that these elements control gene expression via Pol 2 recruitment and/or initiation rather than via promoter proximal pause release. Using genome-wide analysis we show that enhancers, in general, control gene expression at the stage of Pol 2 recruitment and initiation rather than via pausing.
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Project description:Gene transcription occurs via a cycle of linked events including initiation, promoter proximal pausing and elongation of RNA polymerase II (Pol 2). A key question is how do transcriptional enhancers influence these events to control gene expression? Here we have used a new approach to quantify transcriptional initiation and pausing in-vivo, while simultaneously identifying transcription start sites (TSSs) and pause-sites (TPSs). When analysed in parallel with nascent RNA-seq, these data show that differential gene expression is achieved predominantly via changes in transcription initiation rather than Pol 2 pausing or elongation. Using genetically engineered mouse models deleted for specific enhancers we show that these elements control gene expression via Pol 2 recruitment and/or initiation rather than via promoter proximal pause release. Using genome-wide analysis we show that enhancers, in general, control gene expression at the stage of Pol 2 recruitment and initiation rather than via pausing.
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