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Transcription factor occupancy is affected by genetic variation in the white adipose tissue of C57BL6/j and 129S1/SvImJ mice [ChIP-seq]

GSE281685 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 16 samples Submitted 2025/11/12 Platform GPL19057Platform GPL21493
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: 3 × H3K27ac_B6_Chow vs 3 × H3K27ac_SV_Chow vs 3 × H3K27ac_B6_HFD vs 3 × H3K27ac_SV_HFDGroups 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)
Most of the disease associated genetic variants identified in genome wide association studies have been mapped to the non-coding regions of the genome. One of the leading mechanisms by which these variants are thought to affect disease susceptibility is by altering transcription factor (TF) binding. Even though inbred mouse strains have been commonly used to investigate polygenic diseases, less is known on how their genetic differences translate to the level of gene regulation and chromatin landscape.
Read the full summary ↓
Here, we investigated how genetic variation affects chromatin accessibility, a commonly used proxy for TF binding, and how this relates to gene regulation in the epididymal white adipose tissue (eWAT) of C57BL/6J and 129S1/SvImJ mice fed either chow or high-fat diet. We show that differences in chromatin accessibility are almost exclusively strain-specific and driven by genetic variation. In addition, we integrate ATAC-seq (chromatin accessibility) and H3K27ac ChIP-seq (active regulatory regions) data to show that tissue-specific TFs are commonly found in the active regulatory regions hosting TF binding motif altering variants in eWAT. By incorporating footprint analysis, we also show that TF occupancy is consistent with TF binding motif scores at the genetically altered loci. In addition, we validate these findings by extending the footprint analysis to ATAC-seq and H3K27ac ChIP-seq data obtained from the liver. Also, we employ RNA-seq to show that differentially expressed genes are collocated with differentially accessible regions hosting genetic variants. Overall, our findings highlight the connection between differential chromatin accessibility, TF binding and genetic variation and their role in the gene regulation across metabolically central tissues of a mouse model for polygenic obesity.
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 GSE281685_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 PRJNA1185226 and SRA study SRP544757. Searching any of these in the dataset finder brings you back here.

Study design
3 × H3K27ac_B6_Chow vs 3 × H3K27ac_SV_Chow vs 3 × H3K27ac_B6_HFD vs 3 × H3K27ac_SV_HFD

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 16 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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