GEO series

cGAS deficient mice display premature aging associated with loss of chromatin organization, derepression of LINE1 elements and induction of inflammation [RNA-seq]

GSE279025 Mus musculus (mouse) RNA-seq (gene expression) 11 samples Submitted 2026/07/14 Platform GPL24247

At a glance

RNA-seq (gene expression) · mouse · 11 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: 11 samples: 3 × Lung primary fibroblasts, cGAS KO, female vs 3 × Lung primary fibroblasts, cGAS KO, male vs 3 × Lung primary fibroblasts, WT, male vs 2 × Lung primary fibroblasts, WT, femaleGroups 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

Open GSE279025 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 GSE279025_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 PRJNA1169997 and SRA study SRP537172. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

3 × Lung primary fibroblasts, cGAS KO, female vs 3 × Lung primary fibroblasts, cGAS KO, male vs 3 × Lung primary fibroblasts, WT, male vs 2 × Lung primary fibroblasts, WT, female

Supports a between-group comparison across 11 samples.

How we read this: 4 replicated groups read from 11 sample titles; they account for 11 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

GSM8559742 Lung primary fibroblasts, cGAS KO, female 1 Lung primary fibroblast…
GSM8559743 Lung primary fibroblasts, cGAS KO, female 2 Lung primary fibroblast…
GSM8559744 Lung primary fibroblasts, cGAS KO, female 3 Lung primary fibroblast…
GSM8559745 Lung primary fibroblasts, cGAS KO, male 1 Lung primary fibroblast…
GSM8559746 Lung primary fibroblasts, cGAS KO, male 2 Lung primary fibroblast…
GSM8559747 Lung primary fibroblasts, cGAS KO, male 3 Lung primary fibroblast…
GSM8559748 Lung primary fibroblasts, WT, female 1 Lung primary fibroblast…
GSM8559749 Lung primary fibroblasts, WT, female 2 Lung primary fibroblast…
GSM8559750 Lung primary fibroblasts, WT, male 1 Lung primary fibroblast…
GSM8559751 Lung primary fibroblasts, WT, male 2 Lung primary fibroblast…
GSM8559752 Lung primary fibroblasts, WT, male 3 Lung primary fibroblast…

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GSE279026 cGAS deficient mice display premature aging associated with loss of chromatin organization, derepression of LINE1 elements and induction of inflammation 33 samples shares line1, organization, derepression, deficient, premature, chromatin, induction, elements
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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.