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Ubiquitylation of Pol II controls early stages of the transcription cycle [dxChIP-seq]

ABSTRACT: Ubiquitylation of Pol II controls early stages of the transcription cycle [dxChIP-seq]

PROVIDER: PRJNA1156796 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30559921_1.fastq.gz	Fastqsanger.gz
	SRR30559921_2.fastq.gz	Fastqsanger.gz
	SRR30559922_1.fastq.gz	Fastqsanger.gz
	SRR30559922_2.fastq.gz	Fastqsanger.gz
	SRR30559923_1.fastq.gz	Fastqsanger.gz

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Ubiquitylation of Pol II controls early stages of the transcription cycle.

Project description:Ubiquitylation of Pol II controls early stages of the transcription cycle.

| PRJNA1109020 | ENA

Ubiquitylation of Pol II controls early stages of the transcription cycle [TT-seq]

Project description:Control of RNA Polymerase II (Pol II) through ubiquitylation is essential for the DNA-damage response. Here we reveal a distinct ubiquitylation pathway in human cells that targets excessive and defective Pol II molecules at the initial stages of the transcription cycle. This pathway, mediated by ARMC5CUL3 ubiquitin ligase, drives homeostatic Pol II turnover, and is further enhanced when early stages of transcription - initiation and pausing - are perturbed. Upon ARMC5 loss, Pol II accumulates in the free pool and in the promoter-proximal zone, but is not permitted into elongation. We identify Integrator subunit 8 (INTS8) as a gatekeeper preventing the release of excess Pol II molecules into gene bodies. Combined loss of ARMC5 and INTS8 has strong detrimental effects on cell growth, with ARMC5 loss exacerbating transcriptional defects seen in INTS8-depleted cells. These findings uncover that ARMC5CUL3 and INTS8 form a collaborative checkpoint, monitoring the quantity and quality of transcription complexes before they are licensed into elongation.

2024-05-13 | GSE266973 | GEO

Ubiquitylation of Pol II controls early stages of the transcription cycle [dxChIP-seq]

2024-09-07 | GSE276375 | GEO

Ubiquitylation of Pol II controls early stages of the transcription cycle [ChIP-seq]

2024-05-13 | GSE266972 | GEO

Ubiquitylation of Pol II controls early stages of the transcription cycle [ChIP-seq]

Project description:Ubiquitylation of Pol II controls early stages of the transcription cycle [ChIP-seq]

| PRJNA1108872 | ENA

Ubiquitylation of Pol II controls early stages of the transcription cycle [TT-seq]

Project description:Ubiquitylation of Pol II controls early stages of the transcription cycle [TT-seq]

| PRJNA1108871 | ENA

Ubiquitylation of Pol II controls early stages of the transcription cycle.

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-05-13 | GSE266979 | GEO

STK19 drives transcription-coupled nucleotide excision repair by stimulating Pol II ubiquitylation and TFIIH recruitment

Project description:DNA damage forms a major obstacle for gene transcription by RNA polymerase II (Pol II). Transcription-coupled nucleotide excision repair (TC-NER) efficiently eliminates transcription-blocking lesions (TBLs), thereby safeguarding accurate transcription, preserving correct cellular function and counteracting aging. TC-NER initiation involves the recognition of lesion-stalled Pol II by CSB, which recruits the CRL4CSA E3 ubiquitin ligase complex and UVSSA. TBL-induced Pol II ubiquitylation at lysine K1268 by CRL4CSA serves as a critical TC-NER checkpoint, governing Pol II stability and initiating TBL excision by TFIIH recruitment. However, the precise regulatory mechanisms of the CRL4CSA E3 ligase activity and TFIIH recruitment remains elusive. Here, we reveal Serine/Threonine Kinase 19 (STK19) as a novel TC-NER factor. Cryo-EM studies revealed that STK19 is an integral part of the Pol II-TC‐NER complex, bridging CSA with UVSSA, RPB1 and downstream DNA. Live-cell imaging and interaction proteomics shows that STK19 stimulates TC-NER complex stability and proper CRL4CSA complex assembly, resulting in Pol II (K1268) ubiquitylation and subsequent UVSSA and TFIIH recruitment. These findings underscore the crucial role of STK19 as a core component of the TC-NER machinery and its key involvement to the cellular responses to genomic injuries that interfere with transcription.

2024-10-16 | PXD051720 | Pride

ELOF1 anchors CRL4CSA to RNA pol II to activate transcription-coupled repair

Project description:Transcription-coupled DNA repair (TCR) removes transcription-blocking DNA lesions through the coordinated assembly of repair factors on arrested RNA polymerase II (Pol II). This process requires the site-specific ubiquitylation of Pol II by the CRL4CSA ubiquitin ligase. Pol II ubiquitylation is facilitated by ELOF1, a recently identified TCR factor. Using cryogenic electron microscopy, biochemical assays, and cell biology, we reveal that ELOF1 functions as an adaptor to correctly dock CRL4CSA onto Pol II and facilitate the recruitment of UVSSA. The ELOF1-CSA-UVSSA interaction positions CRL4CSA on arrested Pol II, leading to its ubiquitylation upon ligase activation by neddylation. ELOF1-mediated repositioning enables a TFIIS-like element in UVSSA to reach the Pol II active site and the pore region to prevent Pol II re-activation. These findings provide the structural and molecular basis underlying the transition of Pol II from a transcriptionally active to an arrested state, primed for DNA repair.

2023-11-24 | PXD042388 | Pride

Genome-wide profiles of RNA polymerase II (Pol 2) DNA occupancy and the histone modifications H3K4me3 and H3K36me3 around the circadian cycle

Project description:To understand the transcriptional basis of circadian rhythms in mouse liver, we generated genome-wide profiles of RNA polymerase II (Pol 2) DNA occupancy and the histone modifications H3K4me3 and H3K36me3 around the circadian cycle. We found that Pol 2 occupancy at promoters and in gene bodies cycle in synchrony, suggesting that Pol 2 recruitment at promoters underlies circadian gene transcription. On average, Pol 2 occupancy precedes mRNA accumulation by about three hours. Promoters of transcribed genes have tri-methylated H3K4 residues even at their trough activity times, and the tri-methylation levels increase in phase with Pol 2 loading. In contrast, the tri-methylation of H3K36 residues lags transcription by three hours with amplitudes that are markedly shallower, indicating that this mark is less dynamic on the circadian time scale. The comparison of Pol 2 occupancy and mRNA accumulation revealed that both transcriptional and post-transcriptional regulatory mechanisms can account for diurnal mRNA profiles. Additional processed data and visualization tools are available at http://cyclix.vital-it.ch/ Contributed by members of CycliX consortium (http://cyclix.vital-it.ch/) 28 samples examinded, 7 Polr2b, 7 H3K4me3, 7 H3k36me3, 7 input samples.

2012-12-06 | E-GEOD-35788 | biostudies-arrayexpress

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