Sox2 is present in RNA binding complexes and interacts with snRNA 7SK in mouse embryonic stem cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB30572 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR3028470.fastq.gz | Fastqsanger.gz | |||
| ERR3028471.fastq.gz | Fastqsanger.gz | |||
| ERR3028472.fastq.gz | Fastqsanger.gz | |||
| ERR3028473.fastq.gz | Fastqsanger.gz | |||
| ERR3028464.fastq.gz | Fastqsanger.gz |
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Project description:Sox2 is a master transcriptional regulator of embryonic development and has been found to interact with RNA binding proteins such as the non-coding RNA 7SK. 7SK has been shown to regulate transcription at regulatory regions, which could suggest a functional interaction with Sox2 for chromatin recruitment. In this experiment, we assessed chromatin occupancy of 7SK by Chromatin Isolation by RNA Purification (ChIRP) in Sox2 depleted mES cells and found no evidence of Sox2 modulating recruitment of 7SK to chromatin.
2019-05-07 | E-MTAB-7570 | biostudies-arrayexpress
Project description:Eukaryotic genomes are extensively transcribed, but unfettered transcription alters gene expression and leads to genome damage by several means. Divergent transcription occurs at active enhancers and promoters, distinct classes of cis-regulatory elements critical for precise control of gene expression. A key step in RNA Polymerase II (Pol II) transcription is promoter-proximal pausing, which occurs bidirectionally ~25-60 nucleotides downstream of transcription start sites (TSS). Promoter-proximal pause release is gated by the positive transcription elongation factor b (P-TEFb)-7SK snRNA pathway; release from 7SK allows P-TEFb phosphorylation of Pol II and subsequent elongation. The 7SK small nuclear ribonucleoprotein (snRNP) is thought to reside in the nucleoplasm, but it has been suggested that 7SK could operate physically on chromatin. Notably, while enhancer transcription is one of the earliest steps of gene activation and some enhancer RNAs (eRNAs) participate in gene regulation, far less is known about the control of eRNA transcription. Here we show that 7SK inhibits enhancer transcription by modulating nucleosome position. 7SK occupies enhancers and super enhancers genome-wide, and 7SK is required to limit eRNA initiation and synthesis in a manner distinct from promoter pausing. Clustered elements at super enhancers uniquely require 7SK to prevent convergent transcription of colliding polymerases that lead to DNA damage. 7SK inhibits enhancer transcription by modulating chromatin structure, physically interacts with the BAF chromatin remodeling complex, and is required to recruit BAF to enhancers. In turn, 7SK occupancy at enhancers coincides with Brd4 and is exquisitely sensitive to the bromodomain inhibitor JQ1. Thus, 7SK employs distinct mechanisms to counteract diverse consequences of pervasive transcription that distinguish super enhancers, enhancers, and promoters.
2016-02-01 | GSE72599 | GEO
Project description:Eukaryotic genomes are extensively transcribed, but unfettered transcription alters gene expression and leads to genome damage by several means. Divergent transcription occurs at active enhancers and promoters, distinct classes of cis-regulatory elements critical for precise control of gene expression. A key step in RNA Polymerase II (Pol II) transcription is promoter-proximal pausing, which occurs bidirectionally ~25-60 nucleotides downstream of transcription start sites (TSS). Promoter-proximal pause release is gated by the positive transcription elongation factor b (P-TEFb)-7SK snRNA pathway; release from 7SK allows P-TEFb phosphorylation of Pol II and subsequent elongation. The 7SK small nuclear ribonucleoprotein (snRNP) is thought to reside in the nucleoplasm, but it has been suggested that 7SK could operate physically on chromatin. Notably, while enhancer transcription is one of the earliest steps of gene activation12 and some enhancer RNAs (eRNAs) participate in gene regulation, far less is known about the control of eRNA transcription. Here we show that 7SK inhibits enhancer transcription by modulating nucleosome position. 7SK occupies enhancers and super enhancers genome-wide, and 7SK is required to limit eRNA initiation and synthesis in a manner distinct from promoter pausing. Clustered elements at super enhancers uniquely require 7SK to prevent convergent transcription of colliding polymerases. 7SK inhibits enhancer transcription by modulating chromatin structure, physically interacts with the BAF chromatin remodeling complex, and is required to recruit BAF to enhancers. Thus, 7SK employs distinct mechanisms to counteract diverse consequences of pervasive transcription that distinguish super enhancers, enhancers, and promoters
2016-02-01 | GSE69142 | GEO
Project description:Eukaryotic genomes are extensively transcribed, but unfettered transcription alters gene expression and leads to genome damage by several means. Divergent transcription occurs at active enhancers and promoters, distinct classes of cis-regulatory elements critical for precise control of gene expression. A key step in RNA Polymerase II (Pol II) transcription is promoter-proximal pausing, which occurs bidirectionally ~25-60 nucleotides downstream of transcription start sites (TSS). Promoter-proximal pause release is gated by the positive transcription elongation factor b (P-TEFb)-7SK snRNA pathway; release from 7SK allows P-TEFb phosphorylation of Pol II and subsequent elongation. The 7SK small nuclear ribonucleoprotein (snRNP) is thought to reside in the nucleoplasm, but it has been suggested that 7SK could operate physically on chromatin. Notably, while enhancer transcription is one of the earliest steps of gene activation12 and some enhancer RNAs (eRNAs) participate in gene regulation, far less is known about the control of eRNA transcription. Here we show that 7SK inhibits enhancer transcription by modulating nucleosome position. 7SK occupies enhancers and super enhancers genome-wide, and 7SK is required to limit eRNA initiation and synthesis in a manner distinct from promoter pausing. Clustered elements at super enhancers uniquely require 7SK to prevent convergent transcription of colliding polymerases. 7SK inhibits enhancer transcription by modulating chromatin structure, physically interacts with the BAF chromatin remodeling complex, and is required to recruit BAF to enhancers. Thus, 7SK employs distinct mechanisms to counteract diverse consequences of pervasive transcription that distinguish super enhancers, enhancers, and promoters
2016-02-01 | GSE69139 | GEO
Project description:Eukaryotic genomes are extensively transcribed, but unfettered transcription alters gene expression and leads to genome damage by several means. Divergent transcription occurs at active enhancers and promoters, distinct classes of cis-regulatory elements critical for precise control of gene expression. A key step in RNA Polymerase II (Pol II) transcription is promoter-proximal pausing, which occurs bidirectionally ~25-60 nucleotides downstream of transcription start sites (TSS). Promoter-proximal pause release is gated by the positive transcription elongation factor b (P-TEFb)-7SK snRNA pathway; release from 7SK allows P-TEFb phosphorylation of Pol II and subsequent elongation. The 7SK small nuclear ribonucleoprotein (snRNP) is thought to reside in the nucleoplasm, but it has been suggested that 7SK could operate physically on chromatin. Notably, while enhancer transcription is one of the earliest steps of gene activation12 and some enhancer RNAs (eRNAs) participate in gene regulation, far less is known about the control of eRNA transcription. Here we show that 7SK inhibits enhancer transcription by modulating nucleosome position. 7SK occupies enhancers and super enhancers genome-wide, and 7SK is required to limit eRNA initiation and synthesis in a manner distinct from promoter pausing. Clustered elements at super enhancers uniquely require 7SK to prevent convergent transcription of colliding polymerases. 7SK inhibits enhancer transcription by modulating chromatin structure, physically interacts with the BAF chromatin remodeling complex, and is required to recruit BAF to enhancers. Thus, 7SK employs distinct mechanisms to counteract diverse consequences of pervasive transcription that distinguish super enhancers, enhancers, and promoters
2016-02-01 | GSE69141 | GEO
Project description:Eukaryotic genomes are extensively transcribed, but unfettered transcription alters gene expression and leads to genome damage by several means. Divergent transcription occurs at active enhancers and promoters, distinct classes of cis-regulatory elements critical for precise control of gene expression. A key step in RNA Polymerase II (Pol II) transcription is promoter-proximal pausing, which occurs bidirectionally ~25-60 nucleotides downstream of transcription start sites (TSS). Promoter-proximal pause release is gated by the positive transcription elongation factor b (P-TEFb)-7SK snRNA pathway; release from 7SK allows P-TEFb phosphorylation of Pol II and subsequent elongation. The 7SK small nuclear ribonucleoprotein (snRNP) is thought to reside in the nucleoplasm, but it has been suggested that 7SK could operate physically on chromatin. Notably, while enhancer transcription is one of the earliest steps of gene activation12 and some enhancer RNAs (eRNAs) participate in gene regulation, far less is known about the control of eRNA transcription. Here we show that 7SK inhibits enhancer transcription by modulating nucleosome position. 7SK occupies enhancers and super enhancers genome-wide, and 7SK is required to limit eRNA initiation and synthesis in a manner distinct from promoter pausing. Clustered elements at super enhancers uniquely require 7SK to prevent convergent transcription of colliding polymerases. 7SK inhibits enhancer transcription by modulating chromatin structure, physically interacts with the BAF chromatin remodeling complex, and is required to recruit BAF to enhancers. Thus, 7SK employs distinct mechanisms to counteract diverse consequences of pervasive transcription that distinguish super enhancers, enhancers, and promoters
2016-02-01 | GSE69140 | GEO
Project description:Gene expression requires tight coordination of the molecular machineries that mediate transcription and splicing. While the interplay between transcription kinetics and spliceosome fidelity has been investigated before, less is known about mechanisms regulating the assembly of the spliceosomal machinery in response to transcription changes. Here we report an association of the Smn complex, which mediates spliceosomal snRNP biogenesis, with the 7SK complex involved in transcriptional regulation. We found that Smn interacts with the 7SK core components Larp7 and Mepce and specifically associates with 7SK subcomplexes containing hnRNP R. The association between Smn and 7SK complexes is enhanced upon transcriptional inhibition leading to reduced production of snRNPs. Taken together, our findings reveal a functional association of Smn and 7SK complexes that is governed by global changes in transcription. Thus, in addition to its canonical nuclear role in transcriptional regulation, 7SK has cytosolic functions in fine-tuning spliceosome production according to transcriptional demand.
2021-01-26 | PXD021360 | Pride
Project description:Disturbed RNA processing and subcellular transport contribute to the pathomechanisms of motoneuron diseases such as amyotrophic lateral sclerosis and spinal muscular atrophy. RNA-binding proteins are involved in these processes, but the mechanisms how they regulate the subcellular diversity of transcriptomes, in particular in axons, are not understood. hnRNP R interacts with several proteins involved in motoneuron diseases. It is located in axons of developing motoneurons and its depletion causes defects in axon growth. Here, we used iCLIP to determine the RNA interactome of hnRNP R in motoneurons. We identified ~3,500 RNA targets, predominantly with functions in synaptic transmission and axon guidance. Among the RNA targets identified by iCLIP, the non-coding RNA 7SK was the top interactor of hnRNP R. We detected 7SK in the nucleus but also in the cytosol of motoneurons. In axons, 7SK localized in close proximity to hnRNP R and depletion of hnRNP R reduced axonal 7SK. Furthermore, suppression of 7SK led to defective axon growth that was accompanied by axonal transcriptome alterations similar to those caused by hnRNP R depletion. Using a series of 7SK deletion mutants we show that the function of 7SK in axon elongation depends on its interaction with hnRNP R but not with the pTEF-B complex involved in transcriptional regulation. These results propose a role of 7SK as essential interactor of hnRNP R to regulate its function in axon maintenance.
2018-03-06 | GSE77101 | GEO
Project description:The P-TEFb complex promotes transcription elongation by releasing paused RNA polymerase II. P-TEFb itself is known to be inactivated through binding to the non-coding RNA 7SK but there is only limited information about mechanisms regulating their association. Here, we show that cells deficient in the RNA-binding protein hnRNP R, a known 7SK interactor, exhibit increased transcription due to phosphorylation of RNA polymerase II. Intriguingly, loss of hnRNP R promotes the release of P-TEFb from 7SK, accompanied by enhanced hnRNP A1 binding to 7SK. Additionally, we found that hnRNP R interacts with BRD4, and that hnRNP R depletion increases BRD4 binding to the P-TEFb component CDK9. Finally, CDK9 is stabilized upon loss of hnRNP R and its association with Cyclin K is enhanced. Together, our results indicate that hnRNP R negatively regulates transcription by modulating the activity and stability of the P-TEFb complex, exemplifying the multimodal regulation of P-TEFb by an RNA-binding protein.
2022-07-21 | GSE202720 | GEO
Project description:Sox2 has been studied in several types of human solid tumors. The investigators found that Sox2 had higher expression level in colorectal cancer and metastatic tissues than normal tissues. So the investigators assumed that whether Sox2 plays an important role in the progression and migration of colon cancer.
| 2124687 | ecrin-mdr-crc