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Loss of Prom1 triggers RPE Degeneration in Atrophic AMD

GSE298665 Mus musculus (mouse) RNA-seq (gene expression) 15 samples Submitted 2025/12/17 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
Prominin-1 Regulates Retinal Pigment Epithelium Homeostasis: Transcriptomic Insights into Degenerative MechanismsInternational journal of molecular sciences · 2025
Summary (written by the submitters)
The gap in our understanding of the pathobiology of atrophic AMD (aAMD) is a barrier to developing new and effective therapies for geographic atrophy (GA) of the retinal pigment epithelium (RPE). Age-related decline in phagocytic function and impaired autophagy flux in RPE cause oxidized lipid-protein accumulation, accelerating complement-mediated inflammation and leading to RPE cell damage and apoptosis.
Read the full summary ↓
Prominin-1 (Prom1), a glycosylated membrane protein, is essential for photoreceptor (PR) disk biogenesis and outer segment (OS) structure. However, Prom1 mutations are primarily implicated in macular diseases such as Stargardt disease 4 and bull’s eye macular dystrophies. The physiological impact of Prom1 mutations in the retina is not clear. We have shown earlier that Prom1 is a central regulator of autophagy in human RPE and identified Prom1 as an emerging player in RPE homeostasis. We propose to build upon these salient findings by assessing the central hypothesis that Prom1 plays a cell-autonomous role in the RPE and that defects in Prom1-dependent mTORC1-TFEB signaling impair RPE autophagy and lysosomal function, triggering mRPE degeneration and induction of epithelial-mesenchymal transition (EMT). This study investigated whether Prom1 is required for mouse RPE (mRPE) autophagy and phagocytosis, which are cellular processes essential for photoreceptor survival. Prom1-KO decreases autophagy flux, activates mTORC1, and concomitantly decreases transcription factor EB (TFEB) and Cathepsin-D activities in mRPE cells. In addition, Prom1-KO reduces the clearance of bovine photoreceptor outer segments in mRPE cells due to increased mTORC1 and reduced TFEB activities. Dysfunction of Prom1-dependent autophagy correlates with both a decrease in ZO-1 and E-cadherin and a concomitant increase in Vimentin, SNAI1, and ZEB1 levels, consistent with induction of epithelial-mesenchymal transition (EMT) in Prom1-KO mRPE cells. Transcriptomic analysis of Prom1-KO mouse RPE cells by RNA sequencing showed a list of 15 DEGs with high statistical significance in Prom1-KO vs. WT mRPE cells. GSEA and NES show significant upregulation of cell-cycle transcription factors (E2F and MYC targets, G2M checkpoint), mTORC1 signaling, unfolded protein response, reactive oxygen species, TNFA signaling via NF-kappaB, DNA repair, and oxidative phosphorylation pathways; whereas significant downregulation of apical junction and EMT pathways in Prom1-KO vs. WT mRPE cells. Our results demonstrate that Prom1-mTORC1-TFEB signaling is a central driver of cell-autonomous mRPE homeostasis. We show that Prom1-KO in mRPE leads to RPE defects similar to those seen in atrophic age-related macular degeneration and opens new avenues of investigation targeting Prom1 in retinal degenerative diseases.
Published in
Prominin-1 Regulates Retinal Pigment Epithelium Homeostasis: Transcriptomic Insights into Degenerative Mechanisms
Huo W, Yin J, Ghose P et al. · International journal of molecular sciences 2025 · PMID 41373691 · doi:10.3390/ijms262311539
This dataset
Open GSE298665 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 GSE298665_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 PRJNA1270835 and SRA study SRP589480. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41373691) ↗
Study design
5 conditions, mostly in triplicate
WT / 12965-SB ×3 Prom1_KO / 12965-SB ×3 WT / 9262-SB ×3 Prom1_KO / 9262-SB ×3 Prom1_KO / 8995-SB ×2 WT / 8995-SB ×1

Supports a between-group comparison across 14 samples.

How we read this: 5 replicated groups read from 15 sample titles; they account for 14 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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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.