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Interplay between CTCF-binding and CTCF-lacking regulatory elements in generating an architectural stripe at the Igh locus

GSE280719 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 16 samples Submitted 2025/01/21 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: 8 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.
Summary (written by the submitters)
Three-dimensional genome organization orchestrates recombination and transcription of immunoglobulin heavy chain (Igh) genes. The structure of wild type (WT) alleles includes a prominent architectural stripe that extends from a cluster of CTCF binding elements at the 3’ end of the locus (3’CBE), suggesting interactions of this end with sequences throughout the 2Mb Igh TAD.
Read the full summary ↓
Here we elucidate interplay between regulatory elements located in the 3’Igh domain (260 kb) that impact the stripe. The CTCF-lacking intronic enhancer, Eì, promotes stripe formation and tethers sub-TADs between flanking CTCF-bound 3’CBE and IGCR1. Substituting Eì with an EF1á promoter in different orientations partially recapitulates epigenetic features of WT Igh alleles, including active histone modifications, sub-TAD formation and interactions with the 3’CBE, but does not restore VDJ recombination. Loss of IGCR1 increases the stripe while inverting the 3’CBE redirects the stripe away from the Igh locus. However, inverted 3’CBE continue to serve as a boundary against aberrant activation of genes outside the Igh domain by Eì. Our observations provide insights into mechanisms by which regulatory elements modulate chromatin structure and stripe formation.
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 GSE280719_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 PRJNA1180097 and SRA study SRP542213. Searching any of these in the dataset finder brings you back here.

Study design
8 conditions, mostly in duplicate
D345 cells, Nipbl, ChIP, ×2 D345 cells, Wapl, ChIP, ×2 Eu deleted D345 cells, Nipbl, ChIP, ×2 Eu deleted D345 cells,Wapl, ChIP, ×2 Eu replaced with EF1a forward D345 cells, Nip… ×2 Eu replaced with EF1a forward D345 cells, wap… ×2 Eu replaced with EF1a reverse D345 cells, Nip… ×2 Eu replaced with EF1a reverse D345 cells, wap… ×2

Supports a between-group comparison across 16 samples.

How we read this: 8 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
Datasets on a similar topic

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