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TTBK2-Driven Ciliogenesis Is Required for Intrinsic Neuronal Regeneration after Spinal Cord Injury

GSE301749 Mus musculus (mouse) RNA-seq (gene expression) 15 samples Submitted 2026/01/28 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 15 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
15 samples: 5 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.
Paper
TTBK2-Driven Ciliogenesis Is Required for Intrinsic Neuronal Regeneration After Spinal Cord InjuryCNS neuroscience & therapeutics · 2026
Summary (written by the submitters)
Primary cilia (PCs) are microtubule-based organelles that function as critical signaling hubs in both embryonic neurodevelopment and mature neurons. Tau tubulin kinase 2 (TTBK2) is a key initiator of ciliogenesis, but its role in neuronal regeneration following spinal cord injury (SCI) remains unclear. Here, we investigated whether TTBK2 regulates axonal regeneration and circuit remodeling after SCI via a cilia-dependent mechanism.
Read the full summary ↓
Using both in vitro spinal neuron cultures and an in vivo conditional knockout (TTBK2^fl/fl-Cre ERT^+/-) mouse model of T10 spinal hemisection, we demonstrate that TTBK2 deletion impairs PC formation, downregulates Sonic Hedgehog (SHH) signaling, reduces MAP2 expression, and disrupts axonal elongation. Overexpression of TTBK2 rescued these deficits, while loss of ciliary function via KIF3A knockdown replicated the phenotypes. Transcriptomic and proteomic profiling revealed that TTBK2 deficiency suppresses axonogenesis-related pathways while enhancing synaptic excitability markers. Notably, activation of SHH signaling by Smoothened agonist partially restored MAP2 expression and axonal growth in TTBK2-deficient neurons. In vivo, TTBK2 knockout mice displayed impaired motor recovery, increased glial scarring, disrupted axonal projection, and elevated expression of axon growth inhibitors (NogoA/NogoR). Confocal imaging and electron microscopy confirmed the loss of PCs and morphological signs of demyelination and aberrant synaptogenesis. Furthermore, endogenous neural stem cells in TTBK2-deficient mice failed to differentiate into mature neurons, correlating with reduced SHH activity. Collectively, our findings identify a TTBK2–PC–SHH–MAP2 regulatory axis that governs axonal regeneration and circuit reassembly after SCI. This study expands the functional relevance of primary cilia beyond neurodevelopment and highlights TTBK2 as a potential therapeutic target for promoting neural repair in the adult CNS.
Published in
TTBK2-Driven Ciliogenesis Is Required for Intrinsic Neuronal Regeneration After Spinal Cord Injury
Zhang R, Pan S, Tian Z et al. · CNS neuroscience & therapeutics 2026 · PMID 41578860 · doi:10.1002/cns.70763
This dataset
Open GSE301749 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 GSE301749_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1287517 and SRA study SRP598874. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41578860) ↗
Study design
5 conditions, mostly in triplicate
Primary neurons,shControl,Day5 ×3 Primary neurons,shKIF3A,Day5 ×3 Primary neurons,shTTBK2,Day5 ×3 Primary neurons,TTBK2 Overexpress,Day5 ×3 Primary neurons,shKIF3A+TTBK2 Overexpress,Day5 ×3

Supports a case/control comparison: 6 samples read as cases, 3 as controls.

How we read this: 5 replicated groups read from 15 sample titles; they account for 15 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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