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H3K27 and H3K9 Methylation Mask Potential CTCF Binding Sites to Maintain 3D Genome Integrity

GSE293581 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 40 samples Submitted 2025/07/17 Platform GPL21273
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 40 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
40 samples: 20 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
H3K27 and H3K9 methylation mask potential CTCF binding sites to maintain 3D genome integrityGenome research · 2025
Summary (written by the submitters)
The three-dimensional (3D) genome structure is essential for gene regulation and various genomic functions. CTCF plays a key role in organizing Topologically Associated Domains (TADs) and promoter-enhancer loops, contributing to proper cell differentiation and development. Although CTCF binds the genome with high sequence specificity, its binding sites are dynamically regulated during development, and aberrant CTCF binding is linked to diseases such as cancer and neurological disorders, and aging.
Read the full summary ↓
However, the mechanisms controlling CTCF binding remain unclear. Here, we investigated the role of repressive chromatin modifications in CTCF binding using H3K9 methyltransferase-deficient immortalized mouse embryonic fibroblasts (iMEFs) and H3K27 methyltransferase EZH1/2 inhibitor. We found that H3K9 and H3K27 methylation regulate CTCF binding at distinct genomic regions, and their simultaneous loss induces drastic changes in CTCF binding. These changes were associated with alterations in 3D genome architecture and gene expression, suggesting that repressive chromatin modifications preserve proper chromatin organization by preventing aberrant CTCF binding. Additionally, while CTCF binding sites repressed by H3K9 methylation were bound by CTCF in early mouse embryos, those repressed by both H3K9 and H3K27 methylation remained inaccessible, with early embryonic-specific H3K27 methylation forming at these sites. These findings implicate that H3K27 methylation prevents abnormal CTCF binding in early embryos, ensuring proper genome organization during development.
Published in
H3K27 and H3K9 methylation mask potential CTCF binding sites to maintain 3D genome integrity
Fukuda K, Shimura C, Shinkai Y · Genome research 2025 · PMID 40764058 · doi:10.1101/gr.280732.125
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 GSE293581_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 PRJNA1245290 and SRA study SRP576141. Searching any of these in the dataset finder brings you back here.

Study design
20 conditions, mostly in duplicate
CTCF ChIP-seq in WT+DS ×2 CTCF ChIP-seq in 5KOcln14+DS ×2 CTCF ChIP-seq in 5KOcln55+DS ×2 CTCF ChIP-seq in Setdb1KO+DS ×2 CTCF ChIP-seq in TKO+DS ×2 Input ChIP-seq in WT+DS ×2 Input ChIP-seq in 5KOcln14+DS ×2 Input ChIP-seq in 5KOcln55+DS ×2 +12 more

Supports a between-group comparison across 40 samples.

How we read this: 20 replicated groups read from 40 sample titles; they account for 40 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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