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Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulation (Omni-ATAC)

GSE270626 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 20 samples Submitted 2025/02/20 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 20 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
Mus musculus (mouse)
Samples
20 samples: 10 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
Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulationCell genomics · 2025
Summary (written by the submitters)
Here we used a series of CTCF mutations to explore CTCF’s relationship with chromatin and its contribution to gene regulation. CTCF’s impact depends on the genomic context of bound sites and the unique binding properties of WT and mutant CTCF proteins. Specifically, CTCF’s signal strength is linked to changes in accessibility, and the ability to block cohesin is linked to its binding stability.
Read the full summary ↓
Multivariate modelling reveals that both CTCF and accessibility contribute independently to cohesin binding and insulation, however CTCF signal strength has a stronger effect. CTCF and chromatin have a bidirectional relationship such that at CTCF sites, accessibility is reduced in a cohesin-dependent, mutant specific fashion. In addition, each mutant alters TF binding and accessibility in an indirect manner, changes which impart the most influence on rewiring transcriptional networks and the cell’s ability to differentiate. Collectively, the mutant perturbations provide a rich resource for determining CTCF’s site-specific effects.
Published in
Binding domain mutations provide insight into CTCF's relationship with chromatin and its contribution to gene regulation
Do C, Jiang G, Cova G et al. · Cell genomics 2025 · PMID 40118069 · doi:10.1016/j.xgen.2025.100813
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 GSE270626_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 PRJNA1127588. Searching any of these in the dataset finder brings you back here.

Study design
10 conditions, mostly in duplicate
OmniATAC_H455R_ID ×2 OmniATAC_K365T_ID ×2 OmniATAC_Q418R_ID ×2 OmniATAC_R339Q_ID ×2 OmniATAC_R342C_ID ×2 OmniATAC_R377C_ID ×2 OmniATAC_R377H_ID ×2 OmniATAC_R448Q_ID ×2 +2 more

Supports a between-group comparison across 20 samples.

How we read this: 10 replicated groups read from 20 sample titles; they account for 20 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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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.