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Regulation of somatic hypermutation by higher-order chromatin structure [ChIP-Seq]

GSE271542 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 11 samples Submitted 2025/06/16 Platform GPL16791Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 11 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
Homo sapiens (human)
Samples
11 samples: 2 × RAD21-AID c9 4h IAA vs 2 × RAD21-AID c9 8h IAA vs 2 × CTCF vs 2 × RAD21Groups 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
Regulation of somatic hypermutation by higher-order chromatin structureMolecular cell · 2025
Summary (written by the submitters)
The generation of protective antibodies by somatic hypermutation (SHM) is essential for antibody maturation and adaptive immunity. SHM involves co-transcriptional mutagenesis of immunoglobulin variable (V) regions regulated by enhancers located hundreds of kilobases away. How 3D chromatin structure affects SHM is poorly understood. Here, we measure higher-order interactions on single alleles of the human immunoglobulin heavy chain locus (IGH) using Tri-C.
Read the full summary ↓
We find that SHM is underpinned by a multiway hub wherein the V region is proximal to all enhancers. Cohesin-mediated loop extrusion is dispensable for IGH transcription and hub architecture. Transcription and mutagenesis of IGH switch regions, which are necessary for antibody class-switch recombination, creates new chromatin loops that can form without cohesin. However, these additional loops do not compromise hub integrity, V region transcription or SHM. Thus, antibody maturation occurs within a multiway hub accommodating several gene-enhancer loops wherein transcription and mutagenesis of different segments can occur non-competitively.
Published in
Regulation of somatic hypermutation by higher-order chromatin structure
Schoeberl UE, Fitz J, von der Linde M et al. · Molecular cell 2025 · PMID 40580953 · doi:10.1016/j.molcel.2025.06.003
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 GSE271542_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 PRJNA1132194 and SRA study SRP518162. Searching any of these in the dataset finder brings you back here.

Study design
2 × RAD21-AID c9 4h IAA vs 2 × RAD21-AID c9 8h IAA vs 2 × CTCF vs 2 × RAD21

Supports a between-group comparison across 8 samples.

How we read this: 4 replicated groups read from 11 sample titles; they account for 8 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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