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Transcription-Replication conflicts are linked to histone H3K79 methylation and R-loop dependent nucleosome eviction [WGS]

ABSTRACT: Transcription-Replication conflicts are linked to histone H3K79 methylation and R-loop dependent nucleosome eviction [WGS]

PROVIDER: PRJNA1114055 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29101197_1.fastq.gz	Fastqsanger.gz
	SRR29101197_2.fastq.gz	Fastqsanger.gz
	SRR29101198_1.fastq.gz	Fastqsanger.gz
	SRR29101198_2.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcription-Replication conflicts are linked to histone H3K79 methylation and R-loop dependent nucleosome eviction [WGS]

Project description:Transcription-replication conflicts (TRCs) can provoke genome instability. Progressing transcription and replication machineries profoundly impact their underlying chromatin template and thus, conflict sites are vulnerable to chromatin and epigenome alterations. Here, we engineered an inducible TRC reporter system using a genome-integrated R-loop-prone sequence. Using this system, we characterized the dynamic changes of the local chromatin structure inflicted by TRCs, leading to reduced nucleosome occupancy and replication fork blockage. Consequently, inducing a handful TRCs on the genome results in a measurable global replication stress response. We also find a TRC-specific increase in H3K79 methylation at the R-loop forming TRC-site. Accordingly, inhibition of the H3K79 methyltransferase DOT1L leads to increased cellular TRCs and exacerbated DNA damage response, suggesting that deposition of this mark is required for effective detection and resolution of TRCs. Thus, our work highlights the molecular dynamics and reveals specific epigenetic modifiers bookmarking TRC sites, relevant to cancer and other diseases.

2025-05-01 | GSE268016 | GEO

Transcription-Replication conflicts are linked to histone H3K79 methylation and R-loop dependent nucleosome eviction

Project description:Transcription-Replication conflicts are linked to histone H3K79 methylation and R-loop dependent nucleosome eviction

| PRJNA1114052 | ENA

Transcription-Replication conflicts are linked to histone H3K79 methylation and R-loop dependent nucleosome eviction [BrdUseq]

2025-02-26 | GSE267494 | GEO

Transcription-Replication conflicts are linked to histone H3K79 methylation and R-loop dependent nucleosome eviction [ChIPseq]

2025-05-01 | GSE267495 | GEO

Transcription-Replication conflicts are linked to histone H3K79 methylation and R-loop dependent nucleosome eviction [ChIPseq]

Project description:Transcription-Replication conflicts are linked to histone H3K79 methylation and R-loop dependent nucleosome eviction [ChIPseq]

| PRJNA1111581 | ENA

Transcription-Replication conflicts are linked to histone H3K79 methylation and R-loop dependent nucleosome eviction [BrdUseq]

Project description:Transcription-Replication conflicts are linked to histone H3K79 methylation and R-loop dependent nucleosome eviction [BrdUseq]

| PRJNA1111582 | ENA

Transcription-Replication conflicts are linked to histone H3K79 methylation and R-loop dependent nucleosome eviction

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

2025-02-28 | GSE268017 | GEO

Transcription-replication conflicts drive R-loop-dependent nucleosome eviction and require DOT1L activity for transcription recovery

Project description: Not available

| S-EPMC11840560 | biostudies-literature

DDX17 helicase promotes resolution of R-loop-mediated transcription-replication conflicts in human cells

Project description:R-loops are three-stranded nucleic acid structures composed of an RNA:DNA hybrid and displaced DNA strand. These structures can halt DNA replication when formed co- transcriptionally in the opposite orientation to replication fork progression. Recent studies have shown that replication forks stalled by co-transcription R-loops can be restarted by a mechanism involving fork cleavage by MUS81 endonuclease, followed by reactivation of transcription, and fork religation by the DNA ligase IV (LIG4)/XRCC4 complex. However, how R-loops are eliminated to allow the sequential restart of transcription and replication in this pathway remains elusive. Here, we identified the human DDX17 helicase as a factor that associates with R-loops and counteracts R-loop-mediated replication stress to preserve genome stability. We show that DDX17 unwinds RNA:DNA hybrids in vitro and promotes MUS81-dependent restart of R-loop-stalled forks in human cells in a manner dependent on its helicase activity. Loss of DDX17 helicase induces accumulation of R-loops and the formation of R-loop-dependent anaphase bridges and micronuclei. These findings establish DDX17 as a component of the MUS81-LIG4 pathway for resolution of R-loop-mediated transcription- replication conflicts, which may be involved in R-loop unwinding.

2022-11-02 | PXD034331 | Pride

The SWI/SNF chromatin remodeling complex helps resolve R-loop-mediated transcription-replication conflicts

Project description:ATP-dependent chromatin remodelers are commonly mutated in human cancer. Mammalian SWI/SNF complexes comprise three conserved multi-subunit chromatin remodelers (cBAF, ncBAF and PBAF) that share the BRG1 (also known as SMARCA4) subunit responsible for the main ATPase activity. BRG1 is the most frequently mutated Snf2-like ATPase in cancer. Here we have investigated the role of SWI/SNF in genome instability, a hallmark of cancer cells, given its role in transcription, DNA replication and DNA damage repair. We show that depletion of BRG1 increases R-loops and R-loop-dependent DNA breaks, as well as transcription-replication conflicts. BRG1 colocalizes with R-loops and replication fork blocks, as determined by FANCD2 foci, with BRG1 depletion being epistatic to FANCD2 silencing. Our study, extended to other components of SWI/SNF, uncovers a key role of the SWI/SNF complex, in particular cBAF, in helping resolve R-loop-mediated transcription-replication conflicts; thus, unveiling a novel mechanism by which chromatin remodeling protects genome integrity.

2021-05-10 | GSE154631 | GEO

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