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Antagonistic stem cell fates under stress govern decisions between hair greying and melanoma [RNA-seq]

GSE248614 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2025/07/07 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 12 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
12 samples: 3 × Young_telogen vs 3 × Young_early anagen vs 3 × Old_telogen vs 3 × Old_early anagenGroups 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.
Summary (written by the submitters)
The incidence of diseases, including cancer, increases with age. While age-associated diseases with stem cell exhaustion are potentially antagonistic to cancer development1, the relationship between those is still largely unknown. Here, we report that melanocyte stem cells (McSCs) and their niche coordinately govern the antagonism between poliosis (hair graying) and melanoma.
Read the full summary ↓
We found that McSCs undergo senescence-associated differentiation (seno-differentiation) in response to DNA double strand breaks (DSBs) such as by ionizing radiation (IR) and ageing upon their activation for self-renewal, leading to their depletion and resultant hair graying at the cost of cancer protection. RNA-seq and functional analysis of the skin exposed to different types of genotoxic stress revealed that activation of the p53-p21 axis and TBK1 pathway by DSBs within McSCs causes their depletion. Comparative analysis of the young vs. aged stem cell niche identified the KIT ligand (KITL/SCF) as a master niche factor for McSC self-renewal. Strikingly, co-exposure of the irradiated skin to carcinogens rescued hair graying by augmenting the secretory phenotype of niche cells to repress McSC seno-differentiation through the dual activation of KIT signaling and arachidonic acid pathway in McSCs. Collectively, our data provide concrete evidence for the phenotypic trade-off between ageing and cancer based on the niche.
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 GSE248614_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 PRJNA1045037 and SRA study SRP474152. Searching any of these in the dataset finder brings you back here.

Study design
3 × Young_telogen vs 3 × Young_early anagen vs 3 × Old_telogen vs 3 × Old_early anagen

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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.