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Pioneer transcription factor TAL1 reshapes chromatin architecture to direct erythroid cell fate commitment [CUT&Tag]

GSE337274 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 21 samples Submitted 2026/07/06 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 21 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
21 samples: 18 distinct titles, 3 of them repeatedGroups 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)
Pioneer transcription factors critically regulate chromatin organization and hematopoietic cell lineage commitment. During erythropoiesis, hematopoietic stem cells undergo dynamic transcriptional and chromatin remodeling to differentiate into erythrocytes. Functionally validated pioneer factors capable of orchestrating erythropoiesis through dynamic chromatin remodeling remain limited, leaving their regulatory mechanisms incompletely resolved.
Read the full summary ↓
Here, we identify T-cell acute lymphocytic leukemia 1(TAL1) as a pioneer factor that remodels chromatin to drive transcriptional reprogramming during erythropoiesis. By recruiting SWI/SNF complex, TAL1 drives erythroid fate specification while suppressing alternative lineages through lineage-restricted chromatin compartment reorganization. As a pioneer factor, TAL1 recruits chromatin remodelers BPTF and KMT2A to establish erythroid-specific genomic architecture. These complexes collectively execute TAL1 directed differentiation programs by transcriptionally activating erythroid regulators while repressing non-erythroid determinants. Our work establishes a generalizable chromatin accessibility-directed pioneer factor screening strategy, we identify TAL1 as a master pioneer factor and resolve its mechanism in driving erythroid commitment through 3D epigenome restructuring.
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 GSE337274_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 PRJNA1484611 and SRA study SRP714389. Searching any of these in the dataset finder brings you back here.

Study design
18 distinct titles, 3 of them repeated
Erythroid cells, TAL1 Control rep1, Day ×2 Erythroid cells, TAL1 Control rep2, Day ×2 Erythroid cells, TAL1 Control rep3, Day ×2

How we read this: Read from 21 sample titles: 18 distinct titles with little repetition. 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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