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SPG11 organoids reveal lysosomal calcium regulation of neural progenitor proliferation

GSE305269 Homo sapiens (human) RNA-seq (gene expression) 16 samples Submitted 2026/05/29 Platform GPL30173
At a glance

RNA-seq (gene expression) · human · 16 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
Homo sapiens (human)
Samples
16 samples: 4 × Control_NT vs 4 × Control_MLSA vs 4 × SPG11_NT vs 4 × SPG11_MLSAGroups 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
SPG11 models reveal lysosomal calcium regulation of neural progenitor proliferationNeurobiology of disease · 2026
Summary (written by the submitters)
Lysosome dysfunction has been widely implicated in many models of neurodegeneration, but much less is understood of its involvement during brain development in health and disease. Hereditary spastic paraplegia caused by mutations in the SPG11 gene is a neurodevelopmental and neurodegenerative disorder characterized by lysosome dysfunction.
Read the full summary ↓
We identify here lysosomal accumulation of calcium in SPG11 cellular models. We show that alteration of lysosomal calcium reduced proliferation of neural progenitor cells and diminished apical tight junctions in early human cortical development, modeled using organoids derived from induced pluripotent stem cells. The phenotypes were corrected by modulating the lysosomal calcium channel TRPML1 using the drug ML-SA1. We performed RNA-sequencing in control and SPG11 organoids, either untreated or treated with ML-SA1 to identify pathways linking lysosomal dysfunction to proliferation of neural progenitor cells
Published in
SPG11 models reveal lysosomal calcium regulation of neural progenitor proliferation
Samaroo D, Cauhapé M, Bernachot L et al. · Neurobiology of disease 2026 · PMID 42049147 · doi:10.1016/j.nbd.2026.107423
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 GSE305269_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: 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 PRJNA1304967 and SRA study SRP608438. Searching any of these in the dataset finder brings you back here.

Study design
4 × Control_NT vs 4 × Control_MLSA vs 4 × SPG11_NT vs 4 × SPG11_MLSA

Supports a between-group comparison across 16 samples.

How we read this: 4 replicated groups read from 16 sample titles; they account for 16 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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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.