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The PNUTS phosphatase complex controls transcription pause release [ChIP-Seq]

ABSTRACT: Gene expression is regulated by controlling distinct steps of the transcriptional cycle, including initiation, pausing, elongation, and termination. Kinases phosphorylate RNA Polymerase II and associated factors to control transitions between these steps and act as central gene regulatory nodes. Similarly, phosphatases that dephosphorylate these components are emerging as important regulators of transcription, though their roles remain less well understood. Here we discover that the mouse PNUTS-PP1 phosphatase complex plays an essential role in controlling transcription pause release in addition to its previously described function in transcription termination. Transcription pause release by the PNUTS complex is essential for almost all RNA Pol II-dependent gene transcription, relies on its PP1 phosphatase subunit, and controls the phosphorylation of factors required for pause release and elongation. Together, these findings reveal an essential new role for a phosphatase complex in transcription pause release and shows that the PNUTS complex is essential for RNA Pol II-dependent transcription.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE271891 | GEO | 2024/11/26

REPOSITORIES: GEO

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			Action	DRS
		Other
	GSE271891_E14T3G_TND-DD-NTD_mm10_Rep23_MERGED.bw	Other
	GSE271891_E14T3G_TND-DD-T7_mm10_Rep23_MERGED.bw	Other
	GSE271891_E14T3G_W401A-DD-NTD_mm10_Rep23_MERGED.bw	Other
	GSE271891_E14T3G_W401A-DD-T7_mm10_Rep23_MERGED.bw	Other

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The PNUTS phosphatase complex controls transcription pause release [cTT-seq]

Project description:Gene expression is regulated by controlling distinct steps of the transcriptional cycle, including initiation, pausing, elongation, and termination. Kinases phosphorylate RNA Polymerase II and associated factors to control transitions between these steps and act as central gene regulatory nodes. Similarly, phosphatases that dephosphorylate these components are emerging as important regulators of transcription, though their roles remain less well understood. Here we discover that the mouse PNUTS-PP1 phosphatase complex plays an essential role in controlling transcription pause release in addition to its previously described function in transcription termination. Transcription pause release by the PNUTS complex is essential for almost all RNA Pol II-dependent gene transcription, relies on its PP1 phosphatase subunit, and controls the phosphorylation of factors required for pause release and elongation. Together, these findings reveal an essential new role for a phosphatase complex in transcription pause release and shows that the PNUTS complex is essential for RNA Pol II-dependent transcription.

2024-11-26 | GSE271484 | GEO

The PNUTS phosphatase complex controls transcription pause release

Project description:Gene expression is regulated by controlling distinct steps of the transcriptional cycle, including initiation, pausing, elongation, and termination. Kinases phosphorylate RNA Polymerase II and associated factors to control transitions between these steps and act as central gene regulatory nodes. Similarly, phosphatases that dephosphorylate these components are emerging as important regulators of transcription, though their roles remain less well understood. Here we discover that the PNUTS-PP1 phosphatase complex plays an essential role in controlling transcription pause release in addition to its previously described function in transcription termination. Transcription pause release by the PNUTS complex is essential for almost all RNA Pol II-dependent gene transcription, relies on its PP1 phosphatase subunit, and controls the phosphorylation of factors required for pause release and elongation. Together, this reveals an essential new role for a phosphatase complex in transcription pause release and shows that the PNUTS complex is essential for RNA Poll II-dependent transcription.

2024-06-28 | MSV000095177 | MassIVE

Control of RNA pol II speed by PNUTS-PP1 and Spt5 dephosphorylation facilitates termination by a “sitting duck torpedo” mechanism

Project description:Control of transcription speed, which influences many co-transcriptional processes, is poorly understood. We report that PNUTS-PP1 phosphatase is a negative regulator of RNA pol II elongation rate. The PNUTS W401A mutation, which disrupts PP1 binding, causes genome-wide acceleration of transcription associated with hyper-phosphorylation of the Spt5 elongation factor. Immediately downstream of poly(A) sites, pol II decelerates from >2kb/min to <1 kb/min, which correlates with Spt5 dephosphorylation. Pol II deceleration and Spt5 dephosphorylation require poly(A) site recognition and the PNUTS-PP1 complex, which is in turn necessary for transcription termination. These results lead to a new model for termination, the “sitting duck torpedo” mechanism, where poly(A) site-dependent deceleration caused by PNUTS-PP1 and Spt5 dephosphorylation is required to convert pol II into a viable target for the Xrn2 terminator exonuclease. Spt5 and its bacterial homologue NusG therefore have related functions controlling kinetic competition between RNA polymerases and the termination factors that pursue them.

2019-10-30 | GSE134198 | GEO

Restrictor synergizes with Symplekin and PNUTS to terminate extragenic transcription

Project description:Transcription termination pathways mitigate the detrimental consequences of unscheduled promiscuous initiation occurring at hundreds of thousands of genomic cis-regulatory elements. The Restrictor complex, composed of the Pol II-interacting protein WDR82 and the RNA-binding protein ZC3H4, suppresses processive transcription at thousands of extragenic sites in mammalian genomes. Restrictor-driven termination does not involve nascent RNA cleavage and its interplay with other termination machineries is unclear. Here we show that efficient termination at Restrictor-controlled extragenic transcription units involves the recruitment of the protein phosphatase 1 (PP1) regulatory subunit PNUTS, a negative regulator of the Spt5 elongation factor, and Symplekin, a protein associated with RNA cleavage complexes but also involved in cleavage-independent and phosphatase-dependent termination of non-coding RNAs in yeast. PNUTS and Symplekin act synergistically with, but independently from Restrictor to dampen processive extragenic transcription. Moreover, the presence of limiting nuclear levels of Symplekin imposes a competition for its recruitment among multiple transcription termination machineries, resulting in mutual regulatory interactions. Hence, by synergizing with Restrictor, Symplekin and PNUTS enable efficient termination of processive, long-range extragenic transcription.

2024-05-23 | PXD043638 | Pride

The PNUTS-protein phosphatase 1 complex acts as an intrinsic barrier to KSHV replication [eCLIP]

Project description:Control of RNA Polymerase II (pol II) elongation is a critical component of gene expression in mammalian cells. The PNUTS-protein phosphatase 1 (PP1) complex controls elongation rates, slowing pol II after polyadenylation sites to promote termination. The Kaposi's sarcoma-associated herpesvirus (KSHV) co-opts pol II to express its genes, but little is known about its regulation of pol II elongation. We identified PNUTS as a suppressor of a KSHV reporter gene in a genome-wide CRISPR screen. PNUTS depletion also enhances global KSHV gene expression and overall viral replication. Reflecting its host gene activities, PNUTS binds viral RNAs downstream of polyadenylation sites, restricts transcription readthrough of viral genes, and requires PP1 interaction. Surprisingly, PNUTS represses the KSHV reporter by decreasing productive elongation at the 5´-end of the gene. From these data, we conclude that PNUTS' activity forms an intrinsic barrier to KSHV replication likely by suppressing pol II elongation at promoter-proximal regions.

2022-11-19 | GSE201045 | GEO

The PNUTS-protein phosphatase 1 complex acts as an intrinsic barrier to KSHV replication [RNA-seq]

2022-11-19 | GSE201000 | GEO

The PNUTS-protein phosphatase 1 complex acts as an intrinsic barrier to KSHV replication [ChIP-seq]

2022-11-19 | GSE200992 | GEO

The PNUTS-protein phosphatase 1 complex acts as an intrinsic barrier to KSHV replication [CRISPR]

2022-11-19 | GSE200991 | GEO

Knockout of PP1 in Leishmania major reveals a critical role for protein phosphatase 1 during RNA polymerase II transcription termination

Project description:Base J is a modified DNA base that is enriched at RNA polymerase II termination sites. We previously identified a complex in Leishmania major and T. brucei composed of PNUTS, PP1, Wdr82 and a J-binding protein (JBP3). We show that deletion of PP1 in L. major leads to readthrough transcription and expression of downstream genes.

2022-10-01 | GSE200788 | GEO

Base J binding protein (JBP3) is a Component of a Novel Trypanosomatid PNUTS-PP1 Phosphatase Complex involved in RNA Pol II Transcription Termination

Project description:Base J is a modified DNA base that is enriched at RNA polymerase II termination sites and telomeres. We previously found that base J functions to prevent readthrough transcription within gene clusters in T. brucei. We now identify a complex in Leishmania and T. brucei composed of PNUTS, PP1, Wdr82 and a J-binding protein (JBP3). We show the RNAi ablation of PNUTS in T. brucei leads to readthrough transcription and expression of downstream genes.

2020-01-14 | GSE135708 | GEO

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