GEO series

Developmental control of DNA damage responses in α- and β-cells shapes the selective beta-cell susceptibility in diabetes [RNA-Seq]

GSE315104 Mus musculus (mouse) RNA-seq (gene expression) 26 samples Submitted 2026/03/06 Platform GPL17021

At a glance

RNA-seq (gene expression) · mouse · 26 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: 26 samples: 11 × neonatal sample large vs 9 × neonatal sample small vs 6 × adult sampleGroups 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)

Accumulation of DNA damage drives β-cell dysfunction, senescence, and death in Type 1 and Type 2 diabetes. While α-cell dysfunction also contributes to disease pathology, they remain remarkably resistant to senescence and cell-death. The mechanisms underlying these differential responses to diabetogenic stress, particularly differences in their DNA damage vulnerability, remain unclear.

Read the full summary ↓

We demonstrate that replication introduces a window of genomic vulnerability in both α- and β-cells during neonatal growth, with α-cells exhibiting higher replication rates and DNA damage. We show that neonatal β-cells resolve DNA damage more efficiently during mitosis and favor error-free repair, while α-cells compensate for their higher DNA damage vulnerability through increased cellular turnover. Using mouse models of overnutrition and diabetes, we show that β-cells exhibit greater vulnerability to terminal DNA damage and impaired repair capacity under diabetogenic stress, with compensatory replication amplifying this vulnerability. We demonstrate that developmental epigenetic programs shape the differential DNA damage vulnerability of postnatal β- and α-cells. Loss of de novo DNA methyltransferase Dnmt3a in pancreatic progenitors selectively increases the DNA damage vulnerability of β-cells from neonatal growth through adulthood. Our findings uncover novel developmental mechanisms that shape the distinct DNA damage responses of postnatal β- and α-cells during growth and diabetes.

This dataset

Open GSE315104 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 GSE315104_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 PRJNA1395002 and SRA study SRP658569. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

11 × neonatal sample large vs 9 × neonatal sample small vs 6 × adult sample

Supports a between-group comparison across 26 samples.

How we read this: 3 replicated groups read from 26 sample titles; they account for 26 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

GSM9421543 neonatal sample small 1 neonatal sample small
GSM9421544 neonatal sample small 2 neonatal sample small
GSM9421545 neonatal sample small 3 neonatal sample small
GSM9421546 neonatal sample small 4 neonatal sample small
GSM9421547 neonatal sample small 5 neonatal sample small
GSM9421548 neonatal sample small 6 neonatal sample small
GSM9421549 neonatal sample small 7 neonatal sample small
GSM9421550 neonatal sample small 8 neonatal sample small
GSM9421551 neonatal sample small 9 neonatal sample small
GSM9421552 neonatal sample large 10 neonatal sample large
GSM9421553 neonatal sample large 11 neonatal sample large
GSM9421554 neonatal sample large 12 neonatal sample large
GSM9421555 neonatal sample large 13 neonatal sample large
GSM9421556 neonatal sample large 14 neonatal sample large
GSM9421557 neonatal sample large 15 neonatal sample large
GSM9421558 neonatal sample large 16 neonatal sample large
GSM9421559 neonatal sample large 17 neonatal sample large
GSM9421560 neonatal sample large 18 neonatal sample large
GSM9421561 neonatal sample large 19 neonatal sample large
GSM9421562 neonatal sample large 20 neonatal sample large
GSM9421563 adult sample 1 adult sample
GSM9421564 adult sample 2 adult sample
GSM9421565 adult sample 3 adult sample
GSM9421566 adult sample 4 adult sample
GSM9421567 adult sample 5 adult sample
GSM9421568 adult sample 6 adult sample

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GSE271097 Xist RNA targets selective autosomal genes to modulate expression in a Repeat B-dependent manner [RNA-seq] 30 samples shares selective, rna-seq
GSE270456 PHF6 regulates stress susceptibility in the pituitary intermediate lobe [RNA-seq] 24 samples shares susceptibility, rna-seq
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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.