GEO series

CTCF-mediated chromatin topology enables receptor editing to enforce a central B-cell tolerance checkpoint [RNA-seq_IGK repertoire]

GSE313431 Mus musculus (mouse) RNA-seq (gene expression) 10 samples Submitted 2026/01/15 Platform GPL16417

At a glance

RNA-seq (gene expression) · mouse · 10 samples

What it is: RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism: Mus musculus (mouse)
Samples: 10 samples
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)

The generation of a diverse yet self-tolerant B cell repertoire is fundamental to adaptive immunity and is achieved through the ordered process of V(D)J recombination. In mice, Igκ represents the dominant light chain, while Igλ rearrangement serves as a secondary response to nonproductive or autoreactive Igκ recombination — a process known as receptor editing.

Read the full summary ↓

Recombination at the RS element deletes the Igκ constant exon, silencing the locus and enabling Igλ expression. Yet the epigenetic regulatory framework that orchestrates this critical tolerance checkpoint in immature B cells remains unresolved. Here, we identify a CTCF-binding element (CBE) embedded within the 3′-Igκ super-enhancer (3′-SEκ) that governs receptor editing and directs the κ-to-λ switch essential for Igλ⁺ B cell development in vivo. Mechanistically, deletion of this insulator element abrogates chromatin looping essential for receptor editing and concomitantly activates a latent enhancer program within the 3′-SEκ, driving aberrant Vκ recombination and rewiring Igκ chromatin architecture through disrupted CTCF boundary function. Notably, loss of this CBE swiftly leads to elevated autoantibody production, demonstrating that CBE-mediated chromatin architecture shapes B cell fate by constraining autoreactivity. Collectively, these findings establish CTCF-dependent chromatin topology as a checkpoint that couples three-dimensional genome organization with antigen-driven receptor editing, to establish self-tolerance.

This dataset

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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.

Series matrix ↓

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 GSE313431_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

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.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1379500 and SRA study SRP654407. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

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+ 10 more — browse all 10 samples with per-sample file links →

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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.