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H2A.Z reinforces maternal H3K4me3 formation and is essential for meiotic progression in mouse oocytes

GSE262044 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 58 samples Submitted 2025/03/01 Platform GPL19057Platform GPL30172
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 58 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
58 samples: 18 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
H2A.Z reinforces maternal H3K4me3 formation and is essential for meiotic progression in mouse oocytesNature structural & molecular biology · 2025
Summary (written by the submitters)
Mammalian oocytes establish a unique landscape of histone modifications, some of which are inherited by early embryos. How histone variants shape the maternal histone landscape remains unknown. Here, we map histone H2A variants in mouse fully grown oocytes (FGOs) and find that H2A.Z forms broad domains across intergenic regions, along non-canonical H3K4me3 (ncH3K4me3).
Read the full summary ↓
During oocyte growth, H2A.Z progressively transitions from an active promoter-rich, canonical distribution to a non-canonical broad distribution (ncH2A.Z). Depletion of H2A.Z in oocytes partially impairs ncH3K4me3 formation and causes severe defects in meiotic progression, which resemble Mll2-knockout oocytes. Conversely, depletion of ncH3K4me3 by Mll2 knockout also causes a reduction of ncH2A.Z in FGOs. Thus, our study suggests that ncH2A.Z and ncH3K4me3 reinforce each other to form functional oocytes.
Published in
H2A.Z reinforces maternal H3K4me3 formation and is essential for meiotic progression in mouse oocytes
Mei H, Hayashi R, Kozuka C et al. · Nature structural & molecular biology 2025 · PMID 40514539 · doi:10.1038/s41594-025-01573-x
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 GSE262044_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 PRJNA1090085 and SRA study SRP496724. Searching any of these in the dataset finder brings you back here.

Study design
18 conditions, mostly in duplicate
H2A.Z 5d GO ×2 H2A.Z 10d GO ×2 H2A.Z 15d GO ×2 H2A.Z 28d FGO ×2 H2A.Z H2A.Z-CTR FGO ×2 H2A.Z H2A.Z-DKO FGO ×2 H3K4me3 H2A.Z-CTR FGO ×2 H3K4me3 H2A.Z-DKO FGO ×2 +32 more

Supports a case/control comparison: 2 samples read as cases, 5 as controls.

How we read this: 18 replicated groups read from 58 sample titles; they account for 36 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

+ 18 more — browse all 58 samples with per-sample file links →

Datasets on a similar topic

Search all mouse ChIP / ATAC / CUT&Tag datasets in GEO →

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