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Requirements for Establishment and Epigenetic Stability of Mammalian Heterochromatin [ChIP-Seq]

GSE212153 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 18 samples Submitted 2025/09/17 Platform GPL21103
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 18 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
18 samples: 5 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
Requirements for establishment and epigenetic stability of mammalian heterochromatinMolecular cell · 2025
Summary (written by the submitters)
Heterochromatic domains of DNA account for a large fraction of mammalian genomes and have critical roles in silencing of transposons and genes but the mechanisms that establish and maintain these domains are not fully understood. Here we use an inducible heterochromatin formation system combined with targeted CRISPR gene disruption to show that DNA sequence-independent and histone H3 lysine 9 methylation (H3K9me)-dependent heterochromatin can only be inherited during a limited number of cell divisions in mouse embryonic stem cells but becomes stable upon differentiation.
Read the full summary ↓
We show that multiple H3K9 methyltransferases work together with DNA cytosine methyltransferases and other factors, including RNA processing proteins, to establish and maintain heterochromatin. Our findings suggest that components of H3K9 and DNA methylation pathways work in concert to ensure heterochromatin stability.
Published in
Requirements for establishment and epigenetic stability of mammalian heterochromatin
Tatarakis A, Saini H, Yu J et al. · Molecular cell 2025 · PMID 40972525 · doi:10.1016/j.molcel.2025.08.025
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 GSE212153_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 PRJNA874110 and SRA study SRP394290. Searching any of these in the dataset finder brings you back here.

Study design
5 conditions, mostly in duplicate
mESC, H3K9me3, WT, ×2 mESC, H3K9me3, DHX9KO, ×2 mESC, H3K9me3, maintenance, WT, ×2 mESC, H3K9me3, maintenance, DHX9KO, ×2 mESC, H3K9me3, UHRF1KO, ×2 mESC, INPUT (H3K9me3), WT ×1 mESC, INPUT (H3K9me3), DHX9KO ×1 mESC, H3K9me3, before establishment, WT ×1 +5 more

Supports a between-group comparison across 10 samples.

How we read this: 5 replicated groups read from 18 sample titles; they account for 10 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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