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Novel environment exposure drives temporally defined and region-specific chromatin accessibility and gene expression programs in the hippocampus

GSE283483 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 160 samples Submitted 2025/07/16 Platform GPL34328
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 160 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
160 samples: 42 conditions, mostly with about 4 replicates eachGroups 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
Novel environment exposure drives temporally defined and region-specific chromatin accessibility and gene expression changes in the hippocampusNature communications · 2025
Summary (written by the submitters)
Curiosity-driven interactions with novel cues in our environment represent a common behavioral trait across the animal kingdom. Exposure to a novel environment (NE) reshapes the brain via structural and functional changes in multiple brain areas, including the hippocampus. This experience-dependent circuit reorganization is thought to be driven in part by changes in gene expression.
Read the full summary ↓
While substantial progress has been made in generating atlases of cell-type-specific gene expression and chromatin state, these datasets largely reflect conditions in naïve animals, thereby missing transient gene expression programs induced by salient environmental stimuli. NE exposure, for example, has been shown to rapidly induce the expression of Fos and other immediate-early gene transcription factors (IEG TFs). However, the downstream IEG-driven genes (e.g. late response genes, LRGs) that serve to mediate NE-dependent circuit remodeling, as well as the genomic elements that drive the expression of these genes, remain largely unexplored. We employed a combination of single-nucleus multiomics and bulk RNA sequencing of the hippocampal DG, CA3, and CA1 regions to characterize the temporal evolution of cell-type-specific NE-driven gene expression and chromatin accessibility patterns downstream of IEG induction. We observe strong hippocampal regional specificity in excitatory neuron LRG programs, as well as diversity in the inhibitory neuron and non-neuronal transcriptional responses. LRGs were particularly enriched for secreted factors, where we observed cell type-specific expression of their receptors in our snRNA-seq data. These ligands and their cognate receptors represent promising candidates for future study to examine their region- and cell-type-specific effects on learning and memory. In addition, compared to a short exposure, prolonged exposure to NE caused more robust induction of late-response genes, suggesting that sustained environmental stimulation is more effective at triggering the long-lasting molecular changes that support memory formation. In addition, chromatin-level analyses revealed thousands of cell-type-specific changes in chromatin accessibility in response to NE exposure. Coordinated analysis of both chromatin accessibility and gene expression within individual cells revealed the Fos/AP-1 motif as a major predictor of neuronal cell-type-specific LRG expression, suggesting that AP-1 TFs play a regulatory role in NE-driven neuronal gene expression patterns. Together, these data provide a rich resource of hippocampal chromatin accessibility and gene expression profiles in response to novel experience, a physiological stimulus that affects learning and memory.
Published in
Novel environment exposure drives temporally defined and region-specific chromatin accessibility and gene expression changes in the hippocampus
Traunmüller L, Duffy EE, Liu H et al. · Nature communications 2025 · PMID 40841540 · doi:10.1038/s41467-025-63029-6
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 GSE283483_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 PRJNA1192296 and SRA study SRP548421. Searching any of these in the dataset finder brings you back here.

Study design
42 conditions, mostly with about 4 replicates each
CA1_HC ×5 CA1_1h_EE ×5 CA3_HC ×5 CA3_1h_EE ×5 DG_HC ×5 CA1_0.25h_EE ×4 CA1_0.5h_EE ×4 CA1_1.5h_EE ×4 +34 more

Supports a between-group comparison across 160 samples.

How we read this: 42 replicated groups read from 160 sample titles; they account for 160 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

+ 120 more — browse all 160 samples with per-sample file links →

Datasets on a similar topic

Search all mouse ChIP / ATAC / CUT&Tag datasets in GEO →

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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.