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Transcriptional and epigenetic programs of in vitro-expanded HSPCs and their T cell progenitors progeny

GSE286217 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 59 samples Submitted 2026/01/15 Platform GPL30172
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 59 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
59 samples: 25 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)
Hematopoietic stem and progenitor cells (HSPCs) in the bone marrow are the ultimate sources of all hematopoietic lineage cells, including T cells. However, gene expression programs and chromatin dynamics that guide the bone marrow progenitor cells to enter the T-development programs are not fully understood due to limited cell numbers and population heterogeneity.
Read the full summary ↓
By exploiting the in vitro HSPC expansion approach, which effectively expands HSPCs with high T cell potentials, we monitored the gene expression programs and chromatin accessibility changes underlying the transition from the bone marrow progenitor stages to early T cell development stages. Notably, expanded HSPCs displayed strikingly similar chromatin accessibility profiles with early-stage T cell progenitors, representing their shared hematopoietic chromatin landscapes. However, a select set of genomic regions and target genes were specifically regulated as cells first received the strong Notch signaling and engaged with T-development conditions. These events included a robust chromatin opening and transcriptional activation of the T cell receptor (TCR)-C beta locus. In addition, well-known stem and progenitor-associated transcription factors were sharply repressed, often concerted with broad chromatin accessibility losses at those loci. These gene regulation targets were not an artifact of in vitro expanded HSPC-derived pro-T cells. The progeny of expanded HSPCs and freshly isolated HSPCs share the same T-lineage developmental trajectory at the single-cell transcriptome level, and their gene expression programs were highly similar. However, expanded HSPC-derived pro-T cells showed temporal differences in early T-development speed and progressed through pre-commitment stages slowly. From cytokine and chemokine screening, we found that a brief Flt3L pre-treatment during the 4-5 days of the expansion period could moderately accelerate the T-development kinetics of expanded HSPCs. Thus, we compared the chromatin accessibility programs, H3K27ac and H3K27me3 histone marks, and gene expression programs upon Flt3L treatment. Although chromatin state and transcriptional features were mostly not altered by Flt3L treatment at the bulk population levels, scRNA-seq results showed that a set of activation and stress-response genes were upregulated upon Flt3L stimulation. However, Flt3L-primed HSPCs developed through a normal T cell pathway. Together, these datasets (1) provide comprehensive gene expression and chromatin accessibility profiles of expanded HSPCs and their progeny pro-T cells, (2) reveal molecular events accompanied by bone marrow progenitor cells transition to the T cell program, and (3) suggest a slight modification of the expansion protocol for the use of T cell biology studies by adding acute Flt3L treatment.
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 GSE286217_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 PRJNA1208436 and SRA study SRP556249. Searching any of these in the dataset finder brings you back here.

Study design
25 conditions, mostly in duplicate
Expanded_HSPCs_Flt3L_primed_IgG_CnR ×4 Expanded_HSPCs_unprimed_bulk_RNA ×3 Expanded_HSPCs_Flt3L_primed_bulk_RNA ×3 Expanded_HSPCs_unprimed_bulk_ATAC ×3 Expanded_HSPCs_Flt3L_primed_bulk_ATAC ×3 In_vitro_Bcl11bneg_DN2a_bulk_ATAC ×3 Expanded_HSPCs_Sca1+_bulk_RNA ×2 In_vitro_ETP_bulk_RNA_d9 ×2 +19 more

Supports a between-group comparison across 57 samples.

How we read this: 25 replicated groups read from 59 sample titles; they account for 57 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

+ 19 more — browse all 59 samples with per-sample file links →

Datasets on a similar topic

Search all mouse ChIP / ATAC / CUT&Tag datasets in GEO →

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