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 |
Items per page: 5 1 - 2 of 2 |
Similar Datasets
Project description:Analysis of transcription start sites from nascent RNA identifies a unified architecture of initiation at mammalian promoters and enhancers (GRO-cap)
| PRJNA258295 | ENA
Project description:Analysis of transcription start sites from nascent RNA identifies a unified architecture of initiation at mammalian promoters and enhancers (GRO-seq)
| PRJNA258296 | ENA
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.
2014-11-10 | GSE60455 | GEO
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.
2014-11-10 | GSE60454 | GEO
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.
2014-11-10 | GSE60453 | GEO
Project description:Transcription initiation is an essential process for ensuring proper function of any gene, however, we still lack a unified understanding of sequence patterns and rules that explains most transcription initiation sites in human genome. By explaining transcription initiation at basepair resolution from sequence with a deep learning-inspired explainable modeling approach, here we show that simple rules can explain the vast majority of human promoters. We identified key sequence patterns that contribute to human promoter function, each activating transcription with a distinct position-specific effect curve that likely reflects its mechanism of promoting transcription initiation. Most of these position-specific effects have not been previously characterized, and we verified them using experimental perturbations of transcription factor binding sequences. We revealed the sequence basis of bidirectional transcription at promoters and the links between promoter selectivity and gene expression variation across cell types. Additionally, by analyzing 241 mammalian genomes and mouse transcription initiation site data, we showed that the sequence determinants are conserved across mammalian species. Taken together, we provide a unified model for the sequence basis of transcription initiation at basepair resolution(?) that is broadly applicable across mammalian species, which sheds new light on fundamental questions related to promoter sequence and function.
2024-07-10 | GSE248771 | GEO
Project description:Antisense transcription is common at mammalian promoters. Previous studies have largely focused on characterizing antisense transcription initiating upstream of gene transcription start sites. Here, we systematically characterize promoter-proximal antisense transcription downstream of gene transcription starts sites in human T-47D cells, investigating the genomic context of downstream antisense transcription. We find that downstream antisense transcription is widespread, with antisense transcription initiation observed within 2 kb of 28% of gene transcription start sites. Downstream antisense transcription is correlated with many regulatory features at gene promoters despite not being categorically associated with gene activation or repression. At the downstream antisense transcription start site, DNA is accessible, is enriched for protein-associated sequences motifs, and is bound by a variety of transcription factors. Downstream antisense transcription initiates between nucleosomes regularly positioned downstream of gene transcription start sites. Those nucleosomes between gene and downstream antisense transcription start sites carry histone modifications associated with active promoters, such as H3K4me3 and H3K27ac. Strikingly, this same region is bound by chromatin remodeling complexes such as HDAC and SWI/SNF. The coincidence of transcription initiation with nucleosomes displaying promoter-associated histone marks underlies an apparent connection between antisense transcription and the chromatin environment at gene promoters. The association of chromatin remodelers at sites of downstream antisense transcription initiation suggests that antisense transcription contributes to the deposition and maintenance of these chromatin features at gene promoters.
2017-02-11 | GSE74308 | GEO
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.
2021-02-03 | GSE138357 | GEO
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.
2021-02-03 | GSE138356 | GEO