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Exploring the Mechanism of SETDB1 in Regulating Neuroinflammation and Anxiety-Depression-like Behaviors [ATAC-seq]

GSE275351 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 16 samples Submitted 2026/04/04 Platform GPL24676Platform GPL21273Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 16 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
16 samples: 6 conditions, mostly in triplicateGroups 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
SETDB1 modulates neuroinflammation in the mouse cortex by regulating neuronal P2rx7 expressionMolecular psychiatry · 2026
Summary (written by the submitters)
Depression is a globally prevalent disabling mental illness with serious social hazards. Previous studies suggest that neuroinflammation plays an important role in the pathogenesis of depression, but the underlying mechanism remains elusive. Endogenous retrovirus (ERVs) is a type of transposable elements (TEs), consists around 8% of human genome but are mostly silenced in vivo.
Read the full summary ↓
Repressive histone modifications H3K9me3 mediated by the methyltransferase SETDB1 plays a key role in maintaining silencing of ERVs. In this study, we constructed Setdb1-CK-cKO (KO) transgenic mice. Behavioral tests showed that the KO mice exhibited anxiety-depression-like behaviors compared to wild type (WT). Cortex snRNA-seq analysis revealed significant changes in astrocytes in addition to excitatory neurons, with the emergence of a new sub cluster of astrocytes in the KO whose transcriptional profile exhibited specific ERVs activation. We observed a large number of GFAP-positive cells in the KO cortex and striatum by Immunostaining, suggesting reactive astrogliosis. Transcriptomic analysis of astrocytes revealed significant upregulation of genes associated with inflammation in the KO cortex, including multiple chemokine genes. To investigate the potential molecular mechanism underlying "endogenous" neuroinflammation in KO mice, we focused on the purinergic receptor P2X7R, which has been reported to play an important role in mediating neuroinflammation and emotional behaviors. Most importantly, we found that the expression of P2rx7 was significantly upregulated in the KO neuron. We applied multiple epigenomic methods (RNA-seq, ATAC-seq, H3K9me3 ChIP-seq) to analyze in detail the molecular mechanism by which SETDB1 regulates the P2rx7 gene expression, and identified a novel enhancer fragment, mE1. We further constructed a SETDB1 knockout human 293T cell line and examined chromatin accessibility by ATAC-seq. We found a regulatory fragment hE1 with enhancer activity, which was present at a similar location in the human P2RX7 locus, suggesting that this mechanism is conserved between human and mouse. Knockout of P2X7R effectively ameliorated neuroinflammation and partially alleviated neuronal dysfunction as well as behaviors in Setdb1-CK-cKO mice.
Published in
SETDB1 modulates neuroinflammation in the mouse cortex by regulating neuronal P2rx7 expression
Zhu Y, Liao L, Liu X et al. · Molecular psychiatry 2026 · PMID 41935187 · doi:10.1038/s41380-026-03584-6
This dataset
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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 GSE275351_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 PRJNA1150522 and SRA study SRP527773. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41935187) ↗
Study design
6 conditions, mostly in triplicate
Neuron_WT_ATAC ×3 Neuron_KO_ATAC ×3 293T_Ctrl_ATAC ×3 293T_sgSET_ATAC ×3 Astrocyte_WT_ATAC ×2 Astrocyte_KO_ATAC ×2

Supports a between-group comparison across 16 samples.

How we read this: 6 replicated groups read from 16 sample titles; they account for 16 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
Datasets on a similar topic

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