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Mapping of Chromatin Architecture and Enhancer-Promoter Interactions in the Cochlea

GSE305205 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 16 samples Submitted 2025/10/01 Platform 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: 5 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
Mapping of chromatin architecture and enhancer-promoter interactions in the cochleaFrontiers in molecular biosciences · 2025
Summary (written by the submitters)
Chromatin interactions, particularly those between promoters and distal enhancers, enable precise gene regulation in specialized tissues, like the cochlea in the inner ear. Disruptions in these long-range interactions between enhancers and gene promoters are linked to hereditary hearing loss. For many genes important to cochlear development and function, the distal regulatory elements that control their expression remain unknown.
Read the full summary ↓
Identifying these elements and studying their regulatory roles is challenging due to their distance from target genes and the spatial complexity of chromatin architecture. To address this, we employed Micro-C, a high-resolution chromatin conformation capture technique that enables nucleosome-level mapping of chromatin interactions, to construct a cochlea-specific chromatin interaction map. We then integrated epigenomic and transcriptomic data to interpret enhancer-promoter interactions involved in gene regulation.
Published in
Mapping of chromatin architecture and enhancer-promoter interactions in the cochlea
Ege T, Bloom CR, Zhou M et al. · Frontiers in molecular biosciences 2025 · PMID 41169613 · doi:10.3389/fmolb.2025.1683964
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 GSE305205_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 PRJNA1304594 and SRA study SRP608211. Searching any of these in the dataset finder brings you back here.

Study design
5 conditions, mostly with about 4 replicates each
P0 Cochlea ×4 P0 Cochlea CutRun CTCF ×4 P0 Cochlea CutRun H3K4me1 ×3 P0 Cochlea CutRun H3K27ac ×3 P0 Cochlea umiATAC ×2

Supports a between-group comparison across 16 samples.

How we read this: 5 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
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