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The MYCN oncoprotein resolves conflicts of stalling RNA Polymerase with the replication fork [DP_EXOSC10_ChIP_4sUseq]

ABSTRACT: The MYCN oncoprotein resolves conflicts of stalling RNA Polymerase with the replication fork [DP_EXOSC10_ChIP_4sUseq]

PROVIDER: PRJNA691216 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13402800.fastq.gz	Fastqsanger.gz
	SRR13402801.fastq.gz	Fastqsanger.gz
	SRR13402723.fastq.gz	Fastqsanger.gz
	SRR13402724.fastq.gz	Fastqsanger.gz
	SRR13402725.fastq.gz	Fastqsanger.gz

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The MYCN oncoprotein resolves conflicts of stalling RNA Polymerase with the replication fork

Project description:The MYCN oncoprotein resolves conflicts of stalling RNA Polymerase with the replication fork

| PRJNA691219 | ENA

The MYCN oncoprotein resolves conflicts of stalling RNA Polymerase with the replication fork [DP_EXOSC10_Screen]

Project description:During the S-phase, conflicts of replication forks with RNA Polymerase II (RNAPII) threaten genomic stability. While the PAF complex can resolve such conflicts during elongation, the particularly deleterious conflicts with stalling RNAPII are resolved by an as of yet unknown mechanism. Here we show that the MYCN oncoprotein forms a ternary complex with RNAPII and the nuclear RNA exosome, a 3’‑5’ exoribonuclease complex. Together with TFIIS, this complex restarts promoter‑proximal RNAPII, allows escape from co-directional transcription-replication conflicts and prevents double‑strand break accumulation. In cells lacking RNA exosome function, MYCN globally terminates transcription. MYCN-mediated termination is triggered by ATM‑dependent recruitment of BRCA1, which then stabilizes nuclear mRNA decapping complexes. Disruption of mRNA decapping activates ATR, indicative of head-on transcription-replication conflicts, and inhibits DNA replication. We propose that MYCN resolves transcription-replication conflicts via this two-step mechanism to sustain the rapid proliferation of neuroendocrine tumor cells.

2021-12-10 | GSE164568 | GEO

The MYCN oncoprotein resolves conflicts of stalling RNA Polymerase with the replication fork [DP_EXOSC10_BLISS]

2021-12-10 | GSE164567 | GEO

The MYCN oncoprotein resolves conflicts of stalling RNA Polymerase with the replication fork [DP_EXOSC10_ChIP_4sUseq]

2021-12-10 | GSE164555 | GEO

The MYCN oncoprotein resolves conflicts of stalling RNA Polymerase with the replication fork [DP_EXOSC10_Screen]

Project description:The MYCN oncoprotein resolves conflicts of stalling RNA Polymerase with the replication fork [DP_EXOSC10_Screen]

| PRJNA691228 | ENA

The MYCN oncoprotein resolves conflicts of stalling RNA Polymerase with the replication fork [DP_EXOSC10_BLISS]

Project description:The MYCN oncoprotein resolves conflicts of stalling RNA Polymerase with the replication fork [DP_EXOSC10_BLISS]

| PRJNA691227 | ENA

The MYCN oncoprotein resolves conflicts of stalling RNA Polymerase with the replication fork

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

2021-12-10 | GSE164569 | GEO

Characterisation of mRNA expression and replication fork stalling in copper-treated yeast

Project description:Here we analyse steady state mRNA levels and yH2A-marked replication fork stalling sites in S. cerevisiae

2017-05-23 | GSE86283 | GEO

Repression and 3D-restructuring resolves regulatory conflicts in evolutionarily rearranged genomes

Project description:Repression and 3D-restructuring resolves regulatory conflicts in evolutionarily rearranged genomes

| PRJNA770724 | ENA

Genome wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression

Project description:DNA replication progression can be affected by the presence of physical barriers on the DNA, like RNA Polymerases, leading to replication stress and DNA damage. To characterize what happens at sites where DNA replication forks stall and pause, we establish a genome-wide approach to identify them. This approach uses multiple timepoints during S-phase, to identify replication fork/stalling hotspots throughout the genome. These sites are typically associated with increased DNA damage, overlap with fragile sites and with breakpoints of rearrangements identified in cancers, but do not overlap with replication origins. Overlaying these sites with a genome-wide analysis of RNA Polymerase II transcription, we found that replication fork stalling/pausing sites inside genes are directly related to transcription progression and activity. This would support data that indicate that transcription and replication can coexist over the same regions. We found instances where transcription activity by reducing histone density favors replication progression through genes, but also found that slowing down transcription elongation slows down directly replication progression through genes. Importantly, rearrangements found in cancers at transcription-replication collision sites can be detected in non-transformed cells and increased following treatment with ATM and ATR inhibitors. Altogether, our findings highlight how transcription and replication overlap during S-phase, with both positive and negative consequences for replication fork progression and genome stability.

2024-05-13 | GSE169619 | GEO

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