GEO series

Mitochondrial DNA mutation triggers early-onset intestinal epithelial cell dysfunction during acute colitis [mtscATAC-seq]

GSE318907 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 8 samples Submitted 2026/07/30 Platform GPL34290Platform GPL24247

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 8 samples

What it is: ChIP-seq / ATAC-seq (genome binding and open chromatin)Where proteins bind the genome, or which regions are open and active.
Organism: Mus musculus (mouse)
Samples: 8 samples: 8 samples, each with a distinct title — no replicated groupsGroups 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)

Mitochondrial DNA (mtDNA) mutations cause multisystem disorders, involving gastrointestinal (GI) dysfunction. However, the mechanism underlying the selection against mutant mtDNA and the impact of pathogenic mtDNA mutations on intestinal epithelial cells (IECs) remain unclear. Here, we employed mitochondrial single-cell assay for transposase-accessible chromatin with sequencing (mtscATAC-seq) to examine the heteroplasmy of IECs in m.G5081A (mt-tRNA) and m.G12918A (mt-mRNA) mutant mouse models over a two-year lifespan.

Read the full summary ↓

Our findings reveal age-dependent purifying selection against mutant mtDNA across nine IEC subtypes, a process originating in intestinal stem cells (ISCs) that does not strengthen during cellular differentiation. Combining the analysis of single-cell RNA sequencing, we found that young mice with high m.G5081A mutation loads exhibit IEC dysfunction, including impaired enterocyte differentiation and defective Paneth cell granule formation. The m.G5081A mutant mice exhibit increased susceptibility to DSS-induced acute colitis due to compromised intestinal barrier function and impaired wound healing caused by the mtDNA mutation. Collectively, our findings reveal the cellular dynamics of mtDNA selection in IECs and demonstrate the functional consequences of mitochondrial dysfunction on intestinal health, providing insights relevant to mitochondrial disease pathogenesis and management.

This dataset

Open GSE318907 in finder → Find more mouse ChIP / ATAC / CUT&Tag 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 GSE318907_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1420797 and SRA study SRP675879. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

8 samples, each with a distinct title — no replicated groups

Supports a case/control comparison: 7 samples read as cases, 1 as controls.

How we read this: Read from 8 sample titles: 8 distinct titles with little repetition. 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

GSM9505748 TrnA-mutant, 3-week-old, 79% mutation load, mtscATAC-seq
GSM9505749 TrnA-mutant, 55-week-old, 82% mutation load, mtscATAC-seq
GSM9505750 TrnA-mutant, 25-week-old, 78% mutation load, mtscATAC-seq
GSM9505751 TrnA-mutant, 100-week-old, 84% mutation load, mtscATAC-seq
GSM9505752 Wild-type, 25-week-old, mtscATAC-seq
GSM9505753 TrnA-mutant, 25-week-old, 80% mutation load, mtscATAC-seq
GSM9505754 ND5-mutant, 3-week-old, 70% mutation load, mtscATAC-seq
GSM9505755 ND5-mutant, 100-week-old, 70% mutation load, mtscATAC-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.