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EBF1 and PAX5 exert dose dependent epigenetic repression of T-lineage potential [ATAC-seq]

GSE295902 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 18 samples Submitted 2025/11/25 Platform GPL19057
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 18 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
18 samples: 9 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.
Paper
B-lineage commitment is dependent on a reversible epigenetic switchGenes & development · 2026
Summary (written by the submitters)
B-lymphocyte development is dependent on the coordinated action of transcription factors controlling the expression of stage and lineage specific genes. To better understand gene regulation and changes in the epigenetic landscape in early B-cell development, we conducted combined SC-RNA/ATAC seq analysis of bone marrow progenitor populations, allowing us to build a developmental trajectory based on changes in epigenetic accessibility.
Read the full summary ↓
This analysis identified a rapid shift in DNA accessibility, where T-lineage primed progenitors gained the epigenetic landscape of B-lymphocytes. The epigenetic switch correlated well with initiation of EBF1 and PAX5 transcription as well as their functional activity. As ectopic expression of EBF1 in Pax5-/- pro-B cells was not sufficient to mediate either the full activation of the B-lineage program of silencing of T-lineage associated genes, we conclude that PAX5 and EBF1 are independently essential for the establishment of the epigenetic landscape in normal B-cell development. This idea was supported by the finding that pro-B cells from mice with combined heterozygote deletion of the Ebf1 and Pax5 genes, carried a non-differentiated epigenetic landscape and expressed T-lineage associated genes. The importance of epigenetic silencing for the preservation of B-cell fate was supported by the finding that inhibition of the histone methylases EZH1 and EZH2 in pro-B cells, allowed for the activation of T-lineage genes and generation of T-lineage cells in response to Notch signaling. Hence, B-lymphoid commitment is associated with a transcription factor dose dependent epigenetic switch, silencing an inherent T-lineage potential in early lymphoid progenitors.
Published in
B-lineage commitment is dependent on a reversible epigenetic switch
Tingvall-Gustafsson J, Hellerstedt K, Ungerbäck J et al. · Genes & development 2026 · PMID 41266087 · doi:10.1101/gad.353002.125
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 GSE295902_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 PRJNA1256763 and SRA study SRP582255. Searching any of these in the dataset finder brings you back here.

Study design
9 conditions, mostly in duplicate
Ebf1KO, Ctrl, ATAC-seq, ×2 Pax5KO, Ctrl, ATAC-seq, ×2 Pax5KO, Ebf1, ATAC-seq, ×2 WT, exvivo, ATAC-seq, ×2 Ebf1+/-Pax5+/-, exvivo, ATAC-seq, ×2 WT, Op9, ATAC-seq, ×2 Ebf1+/-Pax5+/-, Op9, ATAC-seq, ×2 WT, Op9DL1_24h, ATAC-seq, ×2 +1 more

Supports a between-group comparison across 18 samples.

How we read this: 9 replicated groups read from 18 sample titles; they account for 18 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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