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Satb2 gene dosage in cortical projection neurons impacts neuronal maturation and somatosensory processing [CUT&RUN]

GSE283033 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 39 samples Submitted 2025/11/25 Platform GPL19057
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 39 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
39 samples: 13 conditions, mostly in triplicateGroups 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)
SATB2 Associated Syndrome (SAS) is characterized by severe intellectual deficiency (ID) with limited or absence of speech, behavioral problems, and craniofacial abnormalities. It is caused by de novo heterozygote mutations in the Special AT-rich sequence-Binding Protein 2 (SATB2) gene, which encodes a DNA-binding protein involved in chromatin remodeling.
Read the full summary ↓
In the brain, SATB2 expression is mostly restricted to the projection neurons in the cerebral cortex and hippocampus. Much of what is known about SATB2 function in brain development comes from studies using homozygous loss-of-function mutant mice. Nonetheless, the heterozygous loss of SATB2 negatively impacts brain development, as identified in SAS patients. Here, we report a dose-dependent requirement for Satb2 in regulating subtype specification for layer 5 subcerebral and all intra-telencephalic neurons, as a modulator of gene expression, through its binding to gene promoters and enhancers of many ID genes. Consequently, Satb2 haploinsufficiency in humans, and in mice as we show here, results in aberrations of cortical projection axons that impact mouse sensory behavior including discriminative touch and vocalization. Our findings uncover fundamental mechanisms underlying the etiology of SAS.
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 GSE283033_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 PRJNA1191477 and SRA study SRP548061. Searching any of these in the dataset finder brings you back here.

Study design
13 conditions, mostly in triplicate
e12_h3k27acx_bc ×3 e12_h3k4me3x_bc ×3 e12_h3k27me3_bc ×3 e15_gtlhx2xx_bc ×3 p00_wtn_rbcux1xxx_bc ×3 p00_wtn_rbbcl11ax_bc ×3 e13_rbnr2f1x_bc ×3 p00_rbsatb2x_bc ×3 +5 more

Supports a between-group comparison across 39 samples.

How we read this: 13 replicated groups read from 39 sample titles; they account for 39 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
Datasets on a similar topic

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