Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA258480 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1554311.fastq.gz | Fastqsanger.gz | |||
| SRR1554312.fastq.gz | Fastqsanger.gz |
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Project description:Analysis of transcription start sites from nascent RNA identifies a unified architecture of initiation at mammalian promoters and enhancers (GRO-cap)
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Project description:Analysis of transcription start sites from nascent RNA identifies a unified architecture of initiation at mammalian promoters and enhancers (GRO-seq)
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Project description:Despite the conventional distinction between promoters and enhancers, they share many features in mammals, including divergent transcription and similar modes of transcription factor (TF) binding. Here, we examine the architecture of transcription initiation genome-wide through comprehensive mapping of transcription start sites (TSSs) in human lymphoblastoid B-cell (GM12878) and chronic myelogenous leukemic (K562) tier 1, ENCODE cell lines using a nuclear run-on protocol called GRO-cap. This method captures TSSs for both stable and unstable transcripts, thus allowing us to conduct detailed comparisons between thousands of promoters and enhancers in human cells. These analyses reveal a common architecture of initiation at both promoters and enhancers, including tightly spaced (110 bp) divergent initiation that features similar frequencies of core-promoter sequence elements, highly-positioned flanking nucleosomes, and two modes of TF binding. Transcript elongation stability, a feature determined after transcription initiation, provides a more fundamental distinction between promoters and enhancers than the relative abundance of histone modifications and the presence of TFs or coactivators. These results support a unified model of transcription initiation at both promoters and enhancers.
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Project description:Despite the conventional distinction between promoters and enhancers, they share many features in mammals, including divergent transcription and similar modes of transcription factor (TF) binding. Here, we examine the architecture of transcription initiation genome-wide through comprehensive mapping of transcription start sites (TSSs) in human lymphoblastoid B-cell (GM12878) and chronic myelogenous leukemic (K562) tier 1, ENCODE cell lines using a nuclear run-on protocol called GRO-cap. This method captures TSSs for both stable and unstable transcripts, thus allowing us to conduct detailed comparisons between thousands of promoters and enhancers in human cells. These analyses reveal a common architecture of initiation at both promoters and enhancers, including tightly spaced (110 bp) divergent initiation that features similar frequencies of core-promoter sequence elements, highly-positioned flanking nucleosomes, and two modes of TF binding. Transcript elongation stability, a feature determined after transcription initiation, provides a more fundamental distinction between promoters and enhancers than the relative abundance of histone modifications and the presence of TFs or coactivators. These results support a unified model of transcription initiation at both promoters and enhancers.
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Project description:Despite the conventional distinction between promoters and enhancers, they share many features in mammals, including divergent transcription and similar modes of transcription factor (TF) binding. Here, we examine the architecture of transcription initiation genome-wide through comprehensive mapping of transcription start sites (TSSs) in human lymphoblastoid B-cell (GM12878) and chronic myelogenous leukemic (K562) tier 1, ENCODE cell lines using a nuclear run-on protocol called GRO-cap. This method captures TSSs for both stable and unstable transcripts, thus allowing us to conduct detailed comparisons between thousands of promoters and enhancers in human cells. These analyses reveal a common architecture of initiation at both promoters and enhancers, including tightly spaced (110 bp) divergent initiation that features similar frequencies of core-promoter sequence elements, highly-positioned flanking nucleosomes, and two modes of TF binding. Transcript elongation stability, a feature determined after transcription initiation, provides a more fundamental distinction between promoters and enhancers than the relative abundance of histone modifications and the presence of TFs or coactivators. These results support a unified model of transcription initiation at both promoters and enhancers.
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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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