GEO series

H3K27me3 and the PRC1-H2AK119ub pathway cooperatively maintain heterochromatin and transcriptional silencing after the loss of H3K9 methylation [ChIP-seq]

GSE287032 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 20 samples Submitted 2025/08/01 Platform GPL21273

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.

Summary (written by the submitters)

Heterochromatin is a key architectural feature of eukaryotic chromosomes, essential for cell type-specific gene expression and genome stability. In the mammalian nucleus, heterochromatin is segregated from transcriptionally active euchromatic regions (A compartments), forming large, condensed, and inactive nuclear compartments (B compartments).

Read the full summary ↓

However, the mechanisms underlying its spatial organization remain incompletely understood. Histone H3 lysine 9 and lysine 27 trimethylation (H3K9me3 and H3K27me3) are two major epigenetic modifications that enrich constitutive and facultative heterochromatin, respectively. Previously, we found that the redistribution of H3K27me3 following the loss of H3K9 methylation contributes to heterochromatin maintenance, while the simultaneous loss of both H3K27me3 and H3K9 methylation induces heterochromatin decondensation in mouse embryonic fibroblasts. However, nearly all B compartments were preserved despite the loss of these repressive chromatin modifications. These findings suggest that other factors are responsible for maintaining B compartments under these conditions. In this study, we explored the role of another repressive chromatin modification, PRC1-mediated H2A K119 monoubiquitylation (H2AK119ub/uH2A), in maintaining heterochromatin structure following the loss of H3K9/K27 methylation. We found that uH2A and H3K27me3 independently accumulate in the B compartments after the loss of H3K9 methylation in iMEFs and cooperatively maintain heterochromatin. Our data indicates that the PRC1- uH2A pathway contributes to maintain heterochromatin organization following the loss of H3K9/K27 methylation in mammalian cells.

This dataset

Open GSE287032 in finder → Find more mouse 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 GSE287032_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 PRJNA1211020 and SRA study SRP557489. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

10 conditions, mostly in duplicate

H3K27me3 ChIP-seq in 6KO+sh1A iMEFs ×2 Input in 6KO+sh1A iMEFs ×2 uH2A CATCH-seq in WT iMEFs ×2 uH2A CATCH-seq in WT+DS iMEFs ×2 uH2A CATCH-seq in 5KO iMEFs ×2 uH2A CATCH-seq in 5KO+DS iMEFs ×2 Input CATCH-seq in WT iMEFs ×2 Input CATCH-seq in WT+DS iMEFs ×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

GSM8736793 H3K27me3 ChIP-seq in 6KO+sh1A iMEFs rep1 H3K27me3 ChIP-seq in 6K…
GSM8736794 H3K27me3 ChIP-seq in 6KO+sh1A iMEFs rep2 H3K27me3 ChIP-seq in 6K…
GSM8736795 Input in 6KO+sh1A iMEFs rep1 Input in 6KO+sh1A iMEFs
GSM8736796 Input in 6KO+sh1A iMEFs rep2 Input in 6KO+sh1A iMEFs
GSM8736797 uH2A CATCH-seq in WT iMEFs rep1 uH2A CATCH-seq in WT iM…
GSM8736798 uH2A CATCH-seq in WT iMEFs rep2 uH2A CATCH-seq in WT iM…
GSM8736799 uH2A CATCH-seq in WT+DS iMEFs rep1 uH2A CATCH-seq in WT+DS…
GSM8736800 uH2A CATCH-seq in WT+DS iMEFs rep2 uH2A CATCH-seq in WT+DS…
GSM8736801 uH2A CATCH-seq in 5KO iMEFs rep1 uH2A CATCH-seq in 5KO i…
GSM8736802 uH2A CATCH-seq in 5KO iMEFs rep2 uH2A CATCH-seq in 5KO i…
GSM8736803 uH2A CATCH-seq in 5KO+DS iMEFs rep1 uH2A CATCH-seq in 5KO+D…
GSM8736804 uH2A CATCH-seq in 5KO+DS iMEFs rep2 uH2A CATCH-seq in 5KO+D…
GSM8736805 Input CATCH-seq in WT iMEFs rep1 Input CATCH-seq in WT i…
GSM8736806 Input CATCH-seq in WT iMEFs rep2 Input CATCH-seq in WT i…
GSM8736807 Input CATCH-seq in WT+DS iMEFs rep1 Input CATCH-seq in WT+D…
GSM8736808 Input CATCH-seq in WT+DS iMEFs rep2 Input CATCH-seq in WT+D…
GSM8736809 Input CATCH-seq in 5KO iMEFs rep1 Input CATCH-seq in 5KO …
GSM8736810 Input CATCH-seq in 5KO iMEFs rep2 Input CATCH-seq in 5KO …
GSM8736811 Input CATCH-seq in 5KO+DS iMEFs rep1 Input CATCH-seq in 5KO+…
GSM8736812 Input CATCH-seq in 5KO+DS iMEFs rep2 Input CATCH-seq in 5KO+…

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GSE266317 RNA-seq and ChIP-seq analysis of H3K27ac, H3K27me3, H3K9me2, and JMJD1A in 3T3-L1 cells and ChIP-seq analysis of NFIC in imSVF cells. 14 samples shares h3k27me3, h3k9
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GSE297574 H3K9 di-methylation dynamics underlies mouse minor zygotic genome activation [spike-in ChIP-seq of mESC] 64 samples shares h3k9, methylation
GSE296991 H3K9 di-methylation dynamics underlies mouse minor zygotic genome activation [CATCH-seq of early embryo] 23 samples shares h3k9, methylation
GSE277547 A novel histone H3K27 reader, CBFA2T2, inhibits H3K27me3 demethylation and tumor growth by regulating metabolic genes and metabolite levels [ChIP-seq II] 19 samples shares h3k27me3, methylation

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