GEO series

Long-term maintenance of H3K27me3 in postmitotic neurons is dispensable for gene expression regulation [ChIP-Seq]

GSE330241 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 16 samples Submitted 2026/05/12 Platform GPL30172Platform GPL19057

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 16 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: 16 samples: 2 × GCP, P7, H3K36me vs 2 × GCP, P7, input for H3K36me vs 2 × GC, P21, H3K36me vs 2 × GC, P21, input for H3K36meGroups 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)

Neuronal maturation is associated with extensive changes in gene expression and 3D chromatin architecture. However, the molecular mechanisms that control the epigenetic landscape in terminally differentiated neurons are poorly understood. Here, we show that maturing neurons undergo a striking increase in the levels of the repressive histone modification H3K27me3 broadly across the genome.

Read the full summary ↓

Using mice with a conditional deletion in the catalytic domain of EZH1, the primary H3K27 methyltransferase in postmitotic neurons, we show that H3K27me3 maintenance depends on EZH1. Strikingly, an almost complete loss of H3K27me3 in postmitotic neurons induces minimal changes in gene expression and chromatin accessibility at 7 months of age. The amino acid composition of EZH1 suggests reduced sensitivity to H3K36 methylation, resulting in distinct activities of EZH1 and EZH2 in different chromatin contexts. Together, our results show that a postmitotic switch from EZH2 to EZH1 establishes novel chromatin domains in neurons with a minimal role in transcriptional maintenance.

This dataset

Open GSE330241 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 GSE330241_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 PRJNA1463204 and SRA study SRP698327. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

2 × GCP, P7, H3K36me vs 2 × GCP, P7, input for H3K36me vs 2 × GC, P21, H3K36me vs 2 × GC, P21, input for H3K36me

Supports a between-group comparison across 8 samples.

How we read this: 4 replicated groups read from 16 sample titles; they account for 8 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

GSM9722302 GCP, P7, H3K36me2 GCP, P7, H3K36me
GSM9722303 GCP, P7, H3K36me3 GCP, P7, H3K36me
GSM9722304 GCP, P7, H3K9me3
GSM9722305 GCP, P7, H3K27ac
GSM9722306 GCP, P7, input for H3K36me2 GCP, P7, input for H3K3…
GSM9722307 GCP, P7, input for H3K36me3 GCP, P7, input for H3K3…
GSM9722308 GCP, P7, input for H3K9me3
GSM9722309 GCP, P7, input for H3K27ac
GSM9722310 GC, P21, H3K36me2 GC, P21, H3K36me
GSM9722311 GC, P21, H3K36me3 GC, P21, H3K36me
GSM9722312 GC, P21, H3K9me3
GSM9722313 GC, P21, H3K27ac
GSM9722314 GC, P21, input for H3K36me2 GC, P21, input for H3K3…
GSM9722315 GC, P21, input for H3K36me3 GC, P21, input for H3K3…
GSM9722316 GC, P21, input for H3K9me3
GSM9722317 GC, P21, input for H3K27ac

Datasets on a similar topic

GSE329815 Long-term maintenance of H3K27me3 in postmitotic neurons is dispensable for gene expression regulation 44 samples shares h3k27me3, maintenance, postmitotic, dispensable, long-term, neurons
GSE262390 Setd2 overexpression rescues bivalent gene expression during SCNT-mediated ZGA by enhancing H3K36me3 at gene bodies and excluding H3K27me3 from promoters [ChIP-seq] 79 samples shares h3k27me3, chip-seq
GSE278811 EZHIP-mediated PRC2 inhibition is required to maintain H3K27me3-dependent imprinting post fertilization [ChIP-Seq] 77 samples shares h3k27me3, chip-seq
GSE190102 Ageing-Related Changes to H3K4me3, H3K27ac and H3K27me3 in Purified Mouse Neurons 43 samples shares h3k27me3, neurons
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, chip-seq
GSE281043 The genome wide mapping of H3K4kme3, H3K27ac and H3K27me3 in Ctcf f/f and Ctcf Δ/Δ CALM-AF10 AML cells [ChiP-seq] 16 samples shares h3k27me3, chip-seq
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, chip-seq
GSE303384 Mechanism of maintenance and establishment of repression by the Mtg16 tumor suppressor [CUT&RUN, ChIP-Seq] 92 samples shares maintenance, chip-seq

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