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Acute hormonal signaling-induced 3D chromatin loop reorganization controls adipocyte thermogenesis [ChIP-seq mouse, CTCF, SMC1, MED1]

GSE301366 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 24 samples Submitted 2026/02/17 Platform GPL34290
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 24 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
24 samples: 12 conditions, mostly in duplicateGroups 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
A conserved hormonal signalling-H2A.Z axis rapidly reorganizes 3D chromatin interactions in adipocyte thermogenesisNature metabolism · 2026
Summary (written by the submitters)
Recent molecular advancements have revolutionized our understanding of the role of three-dimensional (3D) genome organization in gene regulation. Yet, the impact of acute hormonal signaling on reshaping genome structure and its consequences for metabolic processes remain largely unexplored. β3-adrenergic receptor (β3-AR) hormonal signaling is imperative for brown adipose tissue (BAT) thermogenesis.
Read the full summary ↓
Here, we demonstrate that β3-AR signaling induces rapid reorganization of fine-scale genome architecture in murine and human brown adipocytes within four hours. High-resolution Micro-C profiling reveals dynamic chromatin loop formation associated with activation of thermogenic genes. Mechanistically, β3-AR signaling promotes p18Hamlet/SRCAP complex assembly, catalyzing incorporation of the histone variant H2A.Z into nucleosomes. ATAC-sequencing reveals that H2A.Z enhances chromatin accessibility at loop anchors, supporting loop formation by facilitating the recruitment of looping factors such as the Mediator complex. Disruption of H2A.Z compromises dynamic chromatin looping and transcriptional activation of thermogenic genes in both species. Mice with BAT-specific H2A.Z deficiency exhibit reduced thermogenic activity and impaired glucose tolerance. Revisiting genome-wide association study analysis reveals that H2A.Z-occupied loops are linked to genetic variants associated with obesity and its related metabolic disorders. Together, these findings highlight the rapid adaptability of 3D genome organization to acute β3-AR signaling and its critical role in brown adipocyte thermoregulation.
Published in
A conserved hormonal signalling-H2A.Z axis rapidly reorganizes 3D chromatin interactions in adipocyte thermogenesis
Zhang Y, Zheng R, Tsuji T et al. · Nature metabolism 2026 · PMID 42014869 · doi:10.1038/s42255-026-01510-2
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 GSE301366_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 PRJNA1284857 and SRA study SRP596427. Searching any of these in the dataset finder brings you back here.

Study design
12 conditions, mostly in duplicate
CTCF, vehicle-treated control BAs ×2 CTCF, β3-AR-stimulated control BAs, ×2 Input for CTCF, vehicle-treated control BAs ×2 Input for CTCF, β3-AR-stimulated control BAs, ×2 Input for MED1, β3-AR-stimulated H2A.Z KD BAs ×2 Input for SMC1 and MED1, vehicle-treated cont… ×2 Input for SMC1 and MED1, β3-AR-stimulated con… ×2 MED1, β3-AR-stimulated H2A.Z KD BAs ×2 +4 more

Supports a between-group comparison across 24 samples.

How we read this: 12 replicated groups read from 24 sample titles; they account for 24 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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