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Mitochondrial fatty acid oxidation regulates monocytic type I interferon signaling via histone acetylation.

GSE279878 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2025/01/07 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 × WT vs 3 × KO vs 3 × LPS/WT vs 3 × LPS/KOGroups 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.
Paper
Mitochondrial fatty acid oxidation regulates monocytic type I interferon signaling via histone acetylationScience advances · 2025
Summary (written by the submitters)
Although lipid-derived acetyl-CoA is a major carbon source for histone acetylation, the contribution of fatty acid -oxidation (FAO) to this process remains poorly characterized. To investigate this, we generated mitochondrial acetyl-CoA acetyltransferase 1 (ACAT1, distal FAO enzyme) knockout macrophages. 13C-carbon tracing confirmed reduced FA-derived carbon incorporation into histone H3 and RNA-seq identified diminished interferon stimulated gene expression in the absence of ACAT1.
Read the full summary ↓
Chromatin accessibility at Stat1 locus was diminished in ACAT1-/- cells. CHIP analysis demonstrated reduced acetyl-H3 binding to Stat1 promoter/enhancer regions and increasing histone acetylation rescued Stat1 expression. IFNβ release was blunted in ACAT1-/- and recovered by ACAT1 reconstitution. Furthermore, ACAT1-dependent histone acetylation required an intact acetylcarnitine shuttle. Finally, obese subjects’ monocytes exhibited increased ACAT1 and histone acetylation levels. Thus, our study identifies a novel link between FAO-mediated epigenetic control of type 1 interferon signaling and uncovers a potential mechanistic link between obesity and type I inferon signaling.
Published in
Mitochondrial fatty acid oxidation regulates monocytic type I interferon signaling via histone acetylation
Wu J, Singh K, Shing V et al. · Science advances 2025 · PMID 39841826 · doi:10.1126/sciadv.adq9301
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 GSE279878_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 PRJNA1175027 and SRA study SRP539542. Searching any of these in the dataset finder brings you back here.

Study design
3 × WT vs 3 × KO vs 3 × LPS/WT vs 3 × LPS/KO

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.