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Cohesin phosphorylation accelerates DNA damage repair and reduces translocations

GSE250510 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 38 samples Submitted 2024/12/05 Platform GPL24676Platform GPL21290Platform GPL34284
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 38 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
38 samples: 16 conditions, mostly in duplicateGroups are read from the sample names, not from the paper. Check the list below.
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
A dual role of Cohesin in DNA DSB repairNature communications · 2025
Summary (written by the submitters)
we describe and clarify several mechanisms whereby Cohesin contributes to DNA repair. Upon acute Cohesin depletion, we observed delayed DNA repair and increased frequency of translocations. These translocations were directly correlated to contact frequency between damaged domains. We found that phosphorylation of the Cohesin subunit SMC1A is required to direct specific Cohesin recruitment at DSBs, without affecting its distribution in the undamaged genome.
Read the full summary ↓
Moreover, Cohesin depletion caused a significant increase in translocations in the 53BP1 deficient background, indicating that Cohesin functions to suppresses 53BP1 independent end joining mechanisms. Our work sheds light on a previously unappreciated mechanisms whereby gCohesin is loaded at DSBs and actively extrudes loops between the break and nearest natural TAD boundary. This process modulates the 3D proximity of broken ends to accelerate repair speeds and prevent long range end joining events during NHEJ.
Published in
A dual role of Cohesin in DNA DSB repair
Fedkenheuer M, Shang Y, Jung S et al. · Nature communications 2025 · PMID 39833168 · doi:10.1038/s41467-025-56086-4
This dataset
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.

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 GSE250510_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1054193 and SRA study SRP478769. Searching any of these in the dataset finder brings you back here.

Study design
16 conditions, mostly in duplicate
Chipseq_Lig4mm_Rad21_DSB ×2 Chipseq_Lig4mm_Rad21_UTR ×2 Chipseq_Pdef_Rad21_DSB ×2 Chipseq_Pdef_Rad21_UTR ×2 Chipseq_WT_Rad21_DSB_ATMi ×2 Chipseq_WT_Rad21_DSB ×2 Chipseq_WT_Rad21_UTR ×2 HIC_WT_DSBAuxin ×2 +14 more

Supports a between-group comparison across 32 samples.

How we read this: 16 replicated groups read from 38 sample titles; they account for 32 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
Datasets on a similar topic

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