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NDF/GLYR1 Promotes RNA Polymerase II Processivity via Pol II Binding and Nucleosome Destabilization

ABSTRACT: NDF/GLYR1 Promotes RNA Polymerase II Processivity via Pol II Binding and Nucleosome Destabilization

PROVIDER: PRJNA1248047 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR33035449.fastq.gz	Fastqsanger.gz
	SRR33035450.fastq.gz	Fastqsanger.gz
	SRR33035453.fastq.gz	Fastqsanger.gz
	SRR33035457.fastq.gz	Fastqsanger.gz

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Similar Datasets

NDF/GLYR1 Promotes RNA Polymerase II Processivity via Pol II Binding and Nucleosome Destabilization

Project description:The Nucleosome Destabilizing Factor (NDF) facilitates transcription through chromatin, but its precise mechanism remains incompletely understood. Here, we identify a critical region (amino acids 140-160) within NDF that specifically interacts with phosphorylated RPB1, the largest subu-nit of elongating RNA Polymerase II (Pol II). Mutations in this region disrupt Pol II interaction and impair Pol II elongation both in vitro and in cells, yet do not affect NDF's ability to destabilize nu-cleosomes, establishing a functional separation between these two activities. Cellular studies re-veal that NDF knockout cells display faster Pol II elongation rates but produce fewer nascent tran-scripts, demonstrating NDF's primary role in maintaining transcriptional processivity through-out gene bodies. Our findings demonstrate that NDF uses distinct mechanisms to ensure productive transcription elongation rather than simply enhancing elongation speed, offering new insights in-to how transcription efficiency is maintained in chromatin.

2025-05-28 | GSE294088 | GEO

NDF/GLYR1 Promotes RNA Polymerase II Processivity via Pol II Binding and Nucleosome Destabilization

2025-05-28 | GSE294087 | GEO

NDF/GLYR1 Promotes RNA Polymerase II Processivity via Pol II Binding and Nucleosome Destabilization

Project description:NDF/GLYR1 Promotes RNA Polymerase II Processivity via Pol II Binding and Nucleosome Destabilization

| PRJNA1248046 | ENA

NDF Is a Transcription Factor that Stimulates Elongation by RNA Polymerase II

Project description:RNA polymerase II (Pol II) elongation is a critical step in gene expression. Here we find that NDF, which was identified as a bilaterian nucleosome-destabilizing factor, is also a Pol II transcription factor that stimulates elongation with plain DNA templates in the absence of nucleosomes. NDF binds directly to Pol II and enhances elongation by a different mechanism than does transcription factor TFIIS. Moreover, yeast Pdp3, which is related to NDF, binds to Pol II and stimulates elongation. Thus, NDF is a Pol II-binding transcription elongation factor that is localized over gene bodies and is conserved from yeast to humans.

2022-03-10 | GSE185464 | GEO

CTDP1 and RPB7 Stabilize Pol II and Permit Reinitiation

Project description:The mechanisms governing the termination and subsequent reinitiation of RNA polymerase II (Pol II) remain poorly understood. Here we found that depletion of RPB7 leads to the destabilization of Pol II’s largest subunit, RPB1. This destabilization is influenced by the loop regions of RPB7, CDK9, the C-terminal domain (CTD) of RPB1, and its linker region. The stabilization process of RPB1 is regulated by the E3 ubiquitin ligase Cullin 3. Additionally, RPB7 interacts with the phosphatase CTDP1, which is crucial for maintaining RPB1 stability. RPB7 is also vital for the reinitiation of Pol II, engages with RNA processing factors, and is localized to the RNA exit channel of the Pol II complex. The absence of RPB7 compromises RNA processing. We propose that RPB7 recruits CTDP1 to dephosphorylate Pol II, enhancing its stability and facilitating efficient reinitiation, adding a new dimension to transcriptional regulation.

2025-02-05 | PXD048909 | Pride

Regulation of RNA polymerase II processivity by Spt5 is restricted to a narrow window in elongation

Project description:Spt5 is a highly conserved RNA polymerase II (Pol II)-associated pausing and elongation factor. However, its impact on global elongation and Pol II processivity in mammalian cells has not been clarified. Here, we show that depleting Spt5 in mouse embryonic fibroblasts (MEFs) does not cause global elongation defects or decreased elongation rates. Instead, in the absence of Spt5, a fraction of Pol II molecules are dislodged during elongation thus decreasing the number of Pol II complexes that complete the transcription cycle. Most strikingly, this decrease is restricted to a narrow window between 15-20 kb from the promoter, a distance which coincides with the stage where accelerating Pol II attains maximum elongation speed and processivity. Consequently, long genes show a greater dependency on Spt5 for optimal elongation efficiency and overall gene expression than short genes. We propose that an important role of Spt5 in mammalian elongation is to promote the processivity of those Pol II complexes that are transitioning towards maximum elongation speed 15-20 kb from the promoter.

2018-03-06 | GSE106313 | GEO

Spt4 promotes Pol I processivity and transcription elongation

Project description:The goal of this study was to determine the effect of Spt4 on transcription by Pol I in vivo. Therefore, Native Elongating Transcript Sequencing (NET-seq) was used to evaluate the occupancy of Pol I in wild-type and spt4△ strains. We determined that in spt4△ yeast, there was a processivity defect and Pol I accumulated at the 5' end of the 35S gene. Additionally, we observed that there was an enrichment for G-rich sequences just downstream of a high A content in the spt4△ strain, indicating that perhaps Spt4 plays a role in helping to propel Pol I through these regions of the rDNA. Altogether, this study suggests that Spt4 is an important transcription factor for Pol I by promoting polymerase processivity.

2021-02-18 | GSE166983 | GEO

Spt4 promotes Pol I processivity and transcription elongation

Project description:Spt4 promotes Pol I processivity and transcription elongation

| PRJNA702517 | ENA

Targeted protein degradation reveals Pol II heterogeneity and functional diversity

Project description:RNA polymerase II (Pol II) subunits are thought to be involved in various transcription-associated processes, but it is unclear whether they play different regulatory roles in modulating gene expression. Here, we performed nascent and mature transcript sequencing after the acute degradation of 12 mammalian Pol II subunits and profiled their genomic binding sites and protein interactomes to dissect their molecular functions. We found that Pol II subunits contribute differently to Pol II cellular localization and transcription process and preferentially regulate RNA processing (such as RNA splicing and 3’ end maturation). Genes sensitive to the depletion of different Pol II subunits tend to be involved in diverse biological functions and show different RNA half-lives. Sequences, associated protein factors, and RNA structures are correlated with Pol II subunit-mediated differential gene expression. These findings collectively suggest that the heterogeneity of Pol II and different genes appear to depend on some of the subunits.

2022-08-09 | PXD035866 |

Stabilization of Pol II protein, orchestration of transcription cycles, and maintenance of enhancer landscape by general transcription regulator SPT5 [ATAC-seq]

Project description:Transcription machinery progression is governed by multitasking regulators including SPT5, an evolutionarily conserved factor implicated in virtually all transcriptional steps from enhancer activation to termination. Yet its mechanistic understanding in human cells remains incomplete. Here we utilize rapid degradation system and reveal crucial function of SPT5 in maintaining cellular and chromatin Pol II levels. Rapid SPT5 depletion causes a pronounced reduction of paused Pol II at promoters and enhancers, distinct from NELF degradation resulting in short-distance paused Pol II redistribution. Most of genes exhibit down- but not upregulation, accompanied by greatly impaired transcription activation and altered chromatin landscape at enhancers, and severe Pol II processivity defects at gene bodies. Phosphorylation of KOWx-4/5- linker potentiates pause release and is antagonized by Integrator-PP2A (INTAC) targeting SPT5 and Pol II. Our findings position SPT5 as an essential positive regulator of global transcription by controlling cellular Pol II levels, enhancer activation and landscape, paused Pol II stability, elongation processivity and termination in human.

2021-09-29 | GSE180844 | GEO

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