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Loss of Neurofascin 186 and Ankyrin G in Purkinje Cells Causes Disruption of Axon Initial Segments, Neurodegeneration and Cerebellar Ataxia

GSE322737 Mus musculus (mouse) RNA-seq (gene expression) 11 samples Submitted 2026/03/27 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 11 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
11 samples: 3 × Control cerebellar hemisphere, biol vs 3 × Pcp2-Cre;NfascFx/Fx cerebellar hemisphere (NF-KO), biol vs 3 × Pcp2-Cre;NfascFx/Fx;AnkGFx/Fx cerebellar hemisphere (Pcp2-DKO), biol vs 2 × Pcp2-Cre;AnkGFx/Fx cerebellar hemisphere (AnkG-KO), biolGroups 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
Purkinje cell-specific loss of Neurofascin and Ankyrin G causes disruption of axon initial segments, neurodegeneration, and cerebellar ataxiaFrontiers in cellular neuroscience · 2026
Summary (written by the submitters)
The axon initial segment (AIS) is essential for initiating action potentials and maintaining neuronal polarity, yet the developmental roles of its core molecular components—Neurofascin 186 (NF186) and Ankyrin G (AnkG)—remain incompletely defined in cerebellar Purkinje cells. Here, we generated Purkinje cell-specific NF186/AnkG double knockout mice to investigate how these adhesion and scaffolding proteins cooperatively regulate AIS formation, ion channel localization, synaptic targeting, and neuronal survival.
Read the full summary ↓
We found that combined deletion of NF186 and AnkG markedly disrupted assembly and maintenance of the AIS cytoskeleton during postnatal development. Other AIS-enriched proteins, including βIV Spectrin (βIVSpec), voltage-gated sodium (Nav) and potassium (Kv1.2) channels, failed to properly localize to the AIS and progressively disintegrated between postnatal days 10 and 30. Notably, Kv1.2 clustering in the pinceau synapse was disrupted, and basket cell axons showed misaligned terminal organization, indicating defective inhibitory synapse innervation. By two months of age, degeneration of Purkinje cells was evident, accompanied by cerebellar dysfunction. In addition, our RNA-seq analysis revealed that Purkinje cell-specific loss of NF186 predominantly activated immune-inflammatory pathways, AnkG loss significantly disrupted neuronal developmental and metabolic processes, and the dual loss of NF186/AnkG produced transcriptional changes that were distinct from, and in part intermediate to, those observed in every single knockout. Collectively, our results show that NF186 and AnkG have complementary, non-redundant roles to establish and maintain the Purkinje cell AIS, and that their loss disrupts synaptic organization at the AIS. These findings advance our understanding of AIS development in cerebellar neurons and have implications for diseases involving AIS dysfunction, including cerebellar ataxia and demyelinating neuropathies.
Published in
Purkinje cell-specific loss of Neurofascin and Ankyrin G causes disruption of axon initial segments, neurodegeneration, and cerebellar ataxia
Shi Q, Taylor AM, Sell LB et al. · Frontiers in cellular neuroscience 2026 · PMID 42052621 · doi:10.3389/fncel.2026.1690466
This dataset
Open GSE322737 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 GSE322737_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 PRJNA1431379 and SRA study SRP680643. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 42052621) ↗
Study design
3 × Control cerebellar hemisphere, biol vs 3 × Pcp2-Cre;NfascFx/Fx cerebellar hemisphere (NF-KO), biol vs 3 × Pcp2-Cre;NfascFx/Fx;AnkGFx/Fx cerebellar hemisphere (Pcp2-DKO), biol vs 2 × Pcp2-Cre;AnkGFx/Fx cerebellar hemisphere (AnkG-KO), biol

Supports a between-group comparison across 11 samples.

How we read this: 4 replicated groups read from 11 sample titles; they account for 11 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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