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CHD7 marks TAD boundaries during neuronal differentiation [Cut & Tag]

GSE293439 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 14 samples Submitted 2025/04/07 Platform GPL21493
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 14 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
14 samples: 14 samples, each with a distinct title — no replicated groupsGroups 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)
The chromodomain helicase DNA binding protein 7 (CHD7) is a nucleosome repositioner implicated in multiple cellular processes, including neuronal differentiation. We identified CHD7 marked sites at TAD boundaries that regulate neuronal differentiation in an otic stem cell line. We showed that CHD7 co-occupied CTCF sites genome-wide. We identified CTCF+ CHD7+ sites near an essential transcription factor, Sox11, required for otic neuronal differentiation.
Read the full summary ↓
The Sox11 promoter and 3’ untranslated region (UTR) showed CHD7 enrichment. The CHD7-marked sites at the 3’UTR displayed histone marks corresponding to active transcription that resulted in Sox11 antisense transcripts. Blocking the singular CHD7-marked site with CRISPRi decreased neurite lengths, reduced neuronal marker expression (TUBB3), and attenuated Sox11 antisense transcripts. Sox11 antisense transcripts were previously suggested to form double-stranded RNA and degrade the Sox11 transcript. Surprisingly, the level of the Sox11 sense transcripts remained unaffected after CRISPRi. We propose that CHD7 at TAD boundaries modulate the chromatin accessibility of CTCF-marked insulators, altering the 3D chromatin organization and ultimately affecting gene expression. Our results implicate a general mechanism of CHD7 in facilitating neuronal differentiation and provide insight into CHD7 dysfunction in CHARGE syndrome, an intellectual developmental disability disorder.
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 GSE293439_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 PRJNA1244626 and SRA study SRP575753. Searching any of these in the dataset finder brings you back here.

Study design
14 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 14 sample titles: 14 distinct titles with little repetition. 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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