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

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

PROVIDER: PRJNA1111581 | ENA |

REPOSITORIES: ENA

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

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 | GSE267495 | 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 [WGS]

2025-05-01 | GSE268016 | GEO

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 [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 [WGS]

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

| PRJNA1114055 | 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

The yeast and human FACT complexes resolve R-loop-mediated transcription-replication conflicts

Project description:Transcription is a major obstacle for replication fork progression and transcription-replication collisions constitute a main cause of genome instability. At a genome-wide scale these obstacles can be detected by the accumulation of the replicative Rrm3 helicase required for RF progression through protein obstacles. Here we show that FACT, a chromatin-reorganizing complex that swaps nucleosomes around the RNA polymerase during transcription elongation and that also has a role in replication, is needed to resolve transcription-replication conflicts in Saccharomyces cerevisiae. Importantly, ChIP-chip analyses of Rrm3 reveal that replication progression impairment in FACT mutants occur genome-wide, but preferentially at highly transcribed regions. ChIP-chip studies were perfomed with antibodies against Rrm3-FLAG in the yeast S. cerevisiae.

2014-03-17 | E-GEOD-51653 | biostudies-arrayexpress

Genome-wide cooperation by HAT Gcn5, remodeler SWI/SNF, and chaperone Ydj1 in promoter nucleosome eviction and transcriptional activation

Project description:Chaperones, nucleosome remodeling complexes and histone acetyltransferases have been implicated in nucleosome disassembly at promoters of particular yeast genes, but whether these co-factors function ubiquitously, and the impact of nucleosome eviction on transcription genome-wide, are poorly understood. We used chromatin immunoprecipitation of histone H3 and RNA polymerase II (Pol II) in mutants lacking single or multiple co-factors to address these issues for ~200 genes belonging to the Gcn4 transcriptome, of which ~70 exhibit marked reductions in H3 promoter occupancy on induction by amino acid starvation. Examining four target genes in a panel of mutants indicated that SWI/SNF, Gcn5, the Hsp70 co-chaperone Ydj1, and chromatin-associated factor Yta7 are required downstream of Gcn4 binding for robust H3 eviction in otherwise wild-type cells. Using ChIP-seq to interrogate all 70 exemplar genes in single, double and triple mutants implicated Gcn5, Snf2 and Ydj1 in H3 eviction at most, but not all Gcn4 target promoters, with Gcn5 generally playing the greatest role and Ydj1 the least. Remarkably, these 3 co-factors cooperate similarly in H3 eviction at virtually all yeast promoters. Defective H3 eviction in co-factor mutants was coupled with reduced Pol II occupancies for the Gcn4 transcriptome and the most highly expressed uninduced genes, but the relative Pol II levels at most genes were unaffected or even elevated. These findings indicate that nucleosome eviction is crucial for robust transcription of highly expressed genes, but that other steps in gene activation are more rate-limiting for most other yeast genes. Chromatin immunoprecipitated DNA from WT (induced(+SM) and uninduced(no SM)) and mutants (induced(+SM)) followed by paired-end sequencing. Nucleosomal DNA obtained by MNase digestion were also subjected to paired-end sequencing.

2015-11-09 | E-GEOD-74787 | biostudies-arrayexpress

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