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Regulation of the RNAPII Pool Is Integral to the DNA Damage Response [TT-seq]

ABSTRACT: Regulation of the RNAPII Pool Is Integral to the DNA Damage Response [TT-seq]

PROVIDER: PRJNA600880 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10876800.fastq.gz	Fastqsanger.gz
	SRR10876801.fastq.gz	Fastqsanger.gz
	SRR10876802.fastq.gz	Fastqsanger.gz
	SRR10876803.fastq.gz	Fastqsanger.gz
	SRR10876804.fastq.gz	Fastqsanger.gz

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Regulation of the RNAPII Pool Is Integral to the DNA Damage Response [TT-seq]

Project description:In response to transcription-blocking DNA damage, cells orchestrate a multi-pronged reaction, involving transcription-coupled DNA repair, degradation of RNAPII and genome-wide transcription shutdown. How these responses are connected has remained unclear. Here we show that damage-induced ubiquitylation of RNAPII itself, at a single lysine (RPB1 K1268), is the focal point for DNA damage response coordination. K1268-ubiquitylation affects DNA repair and signals RNAPII degradation, essential for surviving genotoxic insult. It is also crucial for transcriptional shutdown, in the absence of which cells display dramatic transcriptome alterations. Additionally, regulation of RNAPII stability is central to transcription recovery – indeed, depletion of the RNAPII pool underlies the failure of this process in Cockayne syndrome B cells. These data expose regulation of global RNAPII levels as integral to the cellular DNA damage response, and open the intriguing possibility that RNAPII pool size generally affects cell-specific transcription programmes, in genome instability disorders and even normal cells.

2020-01-14 | GSE143518 | GEO

Regulation of the RNAPII Pool Is Integral to the DNA Damage Response [TT-seq CSBKO]

2020-01-14 | GSE143529 | GEO

Regulation of the RNAPII Pool Is Integral to the DNA Damage Response [TT-seq CSBKO]

Project description:Regulation of the RNAPII Pool Is Integral to the DNA Damage Response [TT-seq CSBKO]

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Regulation of the RNAPII Pool Is Integral to the DNA Damage Response [RNA-seq]

2020-01-14 | GSE143537 | GEO

Regulation of the RNAPII Pool Is Integral to the DNA Damage Response

Project description:Regulation of the RNAPII Pool Is Integral to the DNA Damage Response

| PRJNA600921 | ENA

Regulation of the RNAPII Pool Is Integral to the DNA Damage Response [RNA-seq]

Project description:Regulation of the RNAPII Pool Is Integral to the DNA Damage Response [RNA-seq]

| PRJNA600922 | ENA

Regulation of the RNAPII Pool Is Integral to the DNA Damage Response.

Project description:In response to transcription-blocking DNA damage, cells orchestrate a multi-pronged reaction, involving transcription-coupled DNA repair, degradation of RNA polymerase II (RNAPII), and genome-wide transcription shutdown. Here, we provide insight into how these responses are connected by the finding that ubiquitylation of RNAPII itself, at a single lysine (RPB1 K1268), is the focal point for DNA-damage-response coordination. K1268 ubiquitylation affects DNA repair and signals RNAPII degradation, essential for surviving genotoxic insult. RNAPII degradation results in a shutdown of transcriptional initiation, in the absence of which cells display dramatic transcriptome alterations. Additionally, regulation of RNAPII stability is central to transcription recovery-persistent RNAPII depletion underlies the failure of this process in Cockayne syndrome B cells. These data expose regulation of global RNAPII levels as integral to the cellular DNA-damage response and open the intriguing possibility that RNAPII pool size generally affects cell-specific transcription programs in genome instability disorders and even normal cells.

| S-EPMC7103762 | biostudies-literature

Disruption of RNAPII transcription elongation links Oncogenic splicing factor mutations to replciation stress and targetable alterations in chromatin landscape [TT-TL seq]

Project description:To investigate how whether the RNAPII defect is premature pause release defect or gene body elongation defect due to splicing factor mutations, we peformed TT-TL-seq (TT seq with a time lapse component) in K562 cells (wild type and SF3B1K700E mutant; U2AF1wild type vs U2AF1 S34F mutant) at 4 days after mutant allele expression We then performed metaplot-based and gene expression analysis using data obtained from TT-TL seq

2024-03-12 | GSE225998 | GEO

Regulation of the RNAPII Pool Is Integral to the DNA Damage Response

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

2020-01-14 | GSE143542 | GEO

Bypass of blocking lesions by RNAPII reveals key insights into DNA damage resistance [PRO-seq]

Project description:Ultraviolet (UV) irradiation or platinum-based drugs generate bulky DNA lesions that impede transcription elongation by RNA Polymerase II (RNAPII). This unscheduled transcription elongation block triggers a stress response, which includes initiating transcription-coupled DNA repair, removing and degrading the halted RNAPII, and a global transcriptional shutdown. However, the molecular and cellular consequences of RNAPII successfully bypassing these blocking lesions have remained unknown. Here, we have identified the acetyltransferase p300 as a regulator of the stress response when RNAPII stalls at blocking lesions. Indeed, p300 interacts with the halted RNAPII and controls its removal and degradation in a USP7-dependent mechanism. Notably, in p300-deficient cells, transcription persists despite DNA damage, as RNAPII bypasses blocking lesions, leading to mutant mRNAs and splicing variants accumulation. This persistent transcription activity is particularly detrimental post DNA damage as it results in toxic translation activity and higher DNA damage levels. These observations provide the first evidence that bypass of blocking lesions by RNAPII inhibits DNA repair as well as the cellular stress response. Our findings offer essential insights into the mechanisms of resistance to DNA damage and suggest strategies to enhance the efficacy of platinum-based drugs, such as cisplatin, in anti-tumor therapies.

2025-12-01 | GSE261053 | GEO

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