GEO series

Transcription factor 4 regulates the interhemispheric midline remodeling through neuron–astroglia communications during corpus callosum formation

GSE298404 Mus musculus (mouse) Single-cell RNA-seq 2 samples Submitted 2025/12/04 Platform GPL24247

At a glance

Single-cell RNA-seq · mouse · 2 samples

What it is: Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart. Read from the summary: GEO's own type field only says 'expression profiling by sequencing', so confirm it in the paper.
Organism: Mus musculus (mouse)
Samples: 2 samples
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: Transcription factor 4 regulates the interhemispheric midline remodeling through neuron-astroglia communications during corpus callosum formationTranslational psychiatry · 2025

Summary (written by the submitters)

Agenesis of the corpus callosum (CC), the largest axon tract bridging the two hemispheres of the brain to support higher cognitive functions, is linked to various neurological disorders, including intellectual disability and autism spectrum disorders. Mutations of the transcription factor 4 (TCF4) cause Pitt-Hopkins Syndrome, an autism spectrum brain disorder characterized by severe intellectual disability.

Read the full summary ↓

Through ex vivo transplantation assays and pioneering single-cell RNA sequencing of the interhemispheric midline, we found that Tcf4-mediated neuron-astroglia communication is essential for establishing the midline structure and subsequent CC formation. Conditional inactivation of Tcf4 in guidepost neurons disrupts astroglia functions and impedes interhemispheric fissure closure, thereby preventing axonal crossing of callosal projection neurons to the contralateral cortex. Moreover, we identified Sema7A as a key mediator of neuron-astroglia communications. Therefore, our study reveals a crucial, previously unappreciated role of cell-cell communication in interhemispheric midline remodeling, providing novel insights into the potential mechanisms underlying TCF4 associated neurological disorders.

Published in

Transcription factor 4 regulates the interhemispheric midline remodeling through neuron-astroglia communications during corpus callosum formation

Zeng L, Zhang Y, Zhu Y et al. · Translational psychiatry 2025 · PMID 41253748 · doi:10.1038/s41398-025-03696-7

This dataset

Open GSE298404 in finder → Find more mouse RNA-seq 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 GSE298404_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: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1269090 and SRA study SRP588335. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41253748) ↗

Samples in this study

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+ 2 more — browse all 2 samples with per-sample file links →

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