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Chromatin remodeler CHD7 regulates neurogenic gene expression via controlling chromatin accessibility and modifications of histone marks H3K27me3 and H3K4me3 [Mouse CUT&Tag]

GSE255571 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 10 samples Submitted 2025/08/21 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 10 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
10 samples: 2 × E10.5forbrain_con_CUTTAG_H3K4me3 vs 2 × E10.5forbrain_cKO_CUTTAG_H3K4me3 vs 2 × E10.5forbrain_con_CUTTAG_H3K27me3 vs 2 × E10.5forbrain_cKO_CUTTAG_H3K27me3Groups 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
Mutation of CHD7 impairs the output of neuroepithelium transition that is reversed by the inhibition of EZH2Molecular psychiatry · 2025
Summary (written by the submitters)
CHD7 (Chromo-Helicase-DNA binding protein 7) is an ATP-dependent chromatin remodeler required for neural development. To elucidate the molecular mechanism of the function of CHD7 in neurodevelopment, we performed high-throughput sequencing by RNA-seq, ATAC-seq and CUT&Tag on day 14 human cortical organoids derived from control and CHD7 KO H9 hESCs , as well as RNA-seq and CUT&Tag on E10.5 mouse forebrain which Chd7 was specifically depleted in neuroepithelial cells.
Read the full summary ↓
We found that CHD7 activates neural stem and progenitor cell-specific transcription factors via regulating chromatin accessibility and modification of histone marks H3K27me3 and H3K4me3 in both human cortical organoids and mouse forebrain.
Published in
Mutation of CHD7 impairs the output of neuroepithelium transition that is reversed by the inhibition of EZH2
Huang Z, He C, Wang G et al. · Molecular psychiatry 2025 · PMID 40164694 · doi:10.1038/s41380-025-02990-6
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 GSE255571_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 PRJNA1075462 and SRA study SRP489308. Searching any of these in the dataset finder brings you back here.

Study design
2 × E10.5forbrain_con_CUTTAG_H3K4me3 vs 2 × E10.5forbrain_cKO_CUTTAG_H3K4me3 vs 2 × E10.5forbrain_con_CUTTAG_H3K27me3 vs 2 × E10.5forbrain_cKO_CUTTAG_H3K27me3

Supports a between-group comparison across 8 samples.

How we read this: 4 replicated groups read from 10 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
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