Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA302735 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2925036_1.fastq.gz | Fastqsanger.gz | |||
| SRR2925036_2.fastq.gz | Fastqsanger.gz | |||
| SRR3313640_1.fastq.gz | Fastqsanger.gz | |||
| SRR3313640_2.fastq.gz | Fastqsanger.gz | |||
| SRR3313641_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:Aclarubicin stimulates RNA polymerase II elongation at closely spaced divergent promoters
| PRJNA913597 | ENA
Project description:Transcription is typically divergent, initiating at closely spaced oppositely oriented core promoters to produce sense and unstable upstream antisense transcripts (uasTrx). How antisense transcription is regulated and coordinated with sense transcription is largely unknown. Here by combining acute degradation of the multi-functional transcription factor CTCF and nascent transcription measurements, we find that CTCF specifically suppresses antisense but not sense transcription at hundreds of divergent promoters, the great majority of which bear proximal CTCF binding sites. Genome editing, chromatin conformation studies and 5’ transcript mapping revealed that CTCF directly suppresses uasTrx initiation in manner independent of its chromatin architectural function. Primary transcript RNA FISH revealed co-bursting of sense and anti-sense transcripts is disfavored, suggesting CTCF-regulated competition for transcription initiation. In sum, CTCF shapes the noncoding transcriptional landscape by suppressing upstream antisense transcription.
2022-05-02 | GSE173443 | GEO
Project description:Transcription is typically divergent, initiating at closely spaced oppositely oriented core promoters to produce sense and unstable upstream antisense transcripts (uasTrx). How antisense transcription is regulated and coordinated with sense transcription is largely unknown. Here by combining acute degradation of the multi-functional transcription factor CTCF and nascent transcription measurements, we find that CTCF specifically suppresses antisense but not sense transcription at hundreds of divergent promoters, the great majority of which bear proximal CTCF binding sites. Genome editing, chromatin conformation studies and 5’ transcript mapping revealed that CTCF directly suppresses uasTrx initiation in manner independent of its chromatin architectural function. Primary transcript RNA FISH revealed co-bursting of sense and anti-sense transcripts is disfavored, suggesting CTCF-regulated competition for transcription initiation. In sum, CTCF shapes the noncoding transcriptional landscape by suppressing upstream antisense transcription.
2022-05-02 | GSE173442 | GEO
Project description:Mammalian transcriptomes are complex and formed by extensive promoter activity. Moreover, gene promoters are largely divergent and initiate transcription of reverse-oriented promoter upstream transcripts (PROMPTs). Although PROMPTs are commonly terminated early, influenced by early polyadenylation (pA) sites, promoters often cluster so that the divergent activity of one might impact another. Here, we find that the distance between promoters strongly correlates with the expression, stability and length of their associated PROMPTs. Adjacent promoters driving divergent mRNA transcription support PROMPT formation, but due to pA site constraints, these transcripts tend to spread into the neighboring mRNA on the same strand. This mechanism to derive new alternative mRNA transcription start sites (TSSs) is also evident at closely spaced promoters supporting convergent mRNA transcription. We suggest that basic building blocks of divergently transcribed core promoter pairs, in combination with the wealth of TSSs in mammalian genomes, provides a framework with which evolution shapes transcriptomes.
2016-05-13 | GSE75183 | GEO
Project description:Mammalian transcriptomes are complex and formed by extensive promoter activity. Moreover, gene promoters are largely divergent and initiate transcription of reverse-oriented promoter upstream transcripts (PROMPTs). Although PROMPTs are commonly terminated early, influenced by early polyadenylation (pA) sites, promoters often cluster so that the divergent activity of one might impact another. Here, we find that the distance between promoters strongly correlates with the expression, stability and length of their associated PROMPTs. Adjacent promoters driving divergent mRNA transcription support PROMPT formation, but due to pA site constraints, these transcripts tend to spread into the neighboring mRNA on the same strand. This mechanism to derive new alternative mRNA transcription start sites (TSSs) is also evident at closely spaced promoters supporting convergent mRNA transcription. We suggest that basic building blocks of divergently transcribed core promoter pairs, in combination with the wealth of TSSs in mammalian genomes, provides a framework with which evolution shapes transcriptomes. Mapping of paired 5â?? and 3â??ends of capped and polyadenylated RNAs from RRP40-depleted and eGFP control HeLa cells and using transcript isoform sequencing (TIF-Seq, see Pelechano et al. Nat Protoc 2014 (PMID: 24967623) and Pelechano et al. Nature 2013 (PMID: 23615609)).
2016-05-13 | E-GEOD-75183 | biostudies-arrayexpress
Project description:Nuclear small RNA pathways safeguard genome integrity by establishing transcription-repressing heterochromatin at transposable elements. This inevitably also targets the transposon-rich source loci of the small RNAs themselves. How small RNA source loci are efficiently transcribed while transposon promoters are potently silenced, is not understood. Here, we show that transcription of Drosophila piRNA clusters—small RNA source loci in animal gonads—is enforced through RNA Polymerase II pre-initiation complex formation within repressive heterochromatin. This is accomplished through the TFIIA-L paralog Moonshiner, which is recruited to piRNA clusters via the Heterochromatin Protein-1 variant Rhino. Moonshiner triggers transcription initiation within piRNA clusters by recruiting the TATA box-binding protein (TBP)-related factor TRF2, an animal TFIID core variant. Thus, transcription of heterochromatic small RNA source loci relies on direct recruitment of the core transcriptional machinery to DNA via histone marks rather than sequence motifs, a concept that we argue is a recurring theme in evolution.
2017-08-07 | PXD005026 | Pride
Project description:Spt6 is a conserved factor that controls transcription and chromatin structure across the genome. Although viewed as an elongation factor, spt6 mutations allow transcription from within coding regions, suggesting that Spt6 also controls initiation. To comprehensively characterize the requirement for Spt6 in transcription, we have used four approaches: TSS-seq and TFIIB ChIP-nexus to assay transcription initiation, NET-seq to assay elongating RNAPII, and MNase-seq to assay nucleosome occupancy and positioning. Our results demonstrate that Spt6 represses transcription initiation at thousands of intragenic promoters. We characterize these intragenic promoters, and find some features conserved with genic promoters and other features that are distinct. Finally, we show that Spt6 regulates transcription initiation at most genic promoters and propose a model of initiation site competition to account for this. Together, our results demonstrate that Spt6 controls the fidelity of transcription initiation throughout the genome and reveal the magnitude of the potential for expressing alternative genetic information via intragenic promoters.
2018-11-01 | GSE115775 | GEO
Project description:Cyclin-dependent kinase 7 (CDK7), part of the general transcription factor TFIIH, promotes gene transcription by phosphorylating the C-terminal domain of RNA polymerase II (RNA Pol II). Here, we combine rapid CDK7 kinase inhibition with multi-omics analysis to unravel the direct functions of CDK7 in human cells. CDK7 inhibition causes RNA Pol II retention at promoters, leading to decreased RNA Pol II initiation and immediate global downregulation of transcript synthesis. Elongation, termination, and recruitment of co-transcriptional factors are not directly affected. Although RNA Pol II, initiation factors, and Mediator accumulate at promoters, RNA Pol II complexes can also proceed into gene bodies without promoter-proximal pausing while retaining initiation factors and Mediator. Further downstream, RNA Pol II phosphorylation increases and initiation factors and Mediator are released, allowing recruitment of elongation factors and an increase in RNA Pol II elongation velocity. Collectively, CDK7 kinase activity promotes the release of initiation factors and Mediator from RNA Pol II, facilitating RNA Pol II escape from the promoter.
2024-05-31 | PXD037842 | Pride
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