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GAS deficient mice display premature aging associated with loss of chromatin organization, derepression of LINE1 elements and induction of inflammation [Cut & Tag]

GSE318683 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 14 samples Submitted 2026/07/14 Platform GPL34290
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 14 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
14 samples: 14 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)
Aging-associated inflammation, or ‘inflammaging” is a driver multiple age-associated diseases. Cyclic GMP-AMP Synthase (cGAS) is a cytosolic DNA sensor that functions to activate interferon response upon detecting viral DNA in the cytoplasm. cGAS is also implicated in induction of inflammaging by responding to endogenous signals such as damaged DNA or LINE1 cDNA which forms in aged cells.
Read the full summary ↓
While cGAS knockout mice are viable their aging has not been examined. Unexpectedly, we found that cGAS knockout mice exhibit accelerated aging phenotype associated with induction of inflammation and DNA damage signaling. Cells from cGAS knockout mice showed increased overall chromatin accessibility, particularly on LINE1 (L1) transposons and inflammation genes. Transcription of L1 elements was also increased associated with high levels of cytoplasmic L1 DNA and expression of ORF1 protein. Stimulated emission depletion microscopy (STED) showed that cGAS forms nuclear condensates that co-localize with heterochromatin. Taken together these results suggest a previously undescribed role for cGAS at maintaining heterochromatin and repressing L1 elements. We propose that cGAS knockout mice lose heterochromatin, leading to derepression of L1 elements and induction of inflammation resulting in premature aging phenotype.
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 GSE318683_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1419772 and SRA study SRP675196. Searching any of these in the dataset finder brings you back here.

Study design
14 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 14 sample titles: 14 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
Datasets on a similar topic

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