GEO series

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

GSE267495 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 16 samples Submitted 2025/05/01 Platform GPL24676

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 16 samples

What it is: ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism: Homo sapiens (human)
Samples: 16 samples
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper: Transcription-replication conflicts drive R-loop-dependent nucleosome eviction and require DOT1L activity for transcription recoveryNucleic acids research · 2025

Summary (written by the submitters)

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.

Read the full summary ↓

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.

Published in

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

Werner M, Trauner M, Schauer T et al. · Nucleic acids research 2025 · PMID 39988315 · doi:10.1093/nar/gkaf109

This dataset

Open GSE267495 in finder → Find more human ChIP / ATAC / CUT&Tag datasets →

Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE267495_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1111581 and SRA study SRP507679. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39988315) ↗

Samples in this study

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+ 16 more — browse all 16 samples with per-sample file links →

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