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Asxl1 mutation enhances differentiation in CSF3R-mutated myeloproliferative neoplasms [ATAC-Seq]

GSE266087 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2025/01/22 Platform GPL19057
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 12 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
12 samples: 3 × sgNT/Empty vs 3 × sgB2/Empty vs 3 × sgNT/T618I vs 3 × sgB2/T618IGroups 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
Dual ASXL1 and CSF3R mutations drive myeloid-biased stem cell expansion and enhance neutrophil differentiationBlood advances · 2025
Summary (written by the submitters)
Mutations in the epigenetic regulator Additional Sex Combs-Like 1 (ASXL1) are frequently observed in chronic neutrophilic leukemia (CNL). This disease is classically driven by activating mutations in Colony Stimulating Factor 3 Receptor (CSF3R), which promote the overproduction of neutrophils that characterizes this disease. Despite high rates of co-occurrence, the interplay between ASXL1 and CSF3R mutations in hematopoiesis and leukemia development remains poorly understood.
Read the full summary ↓
Here, we present a new mouse model with both Asxl1Y588X and Csf3rT621I mutations, which recapitulates features of human CNL. Csf3r-mutant mice exhibit an age-associated depletion of hematopoietic stem and progenitor cells, which is reversed by the addition of Asxl1Y588X. This combination of mutations causes an expansion of myeloid-biased stem cells. As the mice age they develop neutrophilia, but leukemia is rare, suggesting additional mutations may be required for transformation. Using models of myeloid differentiation, we find that ASXL1 truncation enhances CSF3RT618I-driven neutrophil differentiation by downregulating MYC programs and activating inflammatory pathways associated with mature myeloid cell production. Moreover, cells with both mutations had increased priming of neutrophil-associated enhancers and reduced priming of enhancers associated with monocytic differentiation. Mutant ASXL1 is known to decrease genome-wide abundance of a repressive histone mark—H2AK119ub. While we see the expected decrease in H2AK119ub in Asxl1-mutant cells, this effect is reversed when CSF3R is also mutated, suggesting a complex interplay between these mutations in regulating chromatin dynamics during hematopoiesis. Our findings highlight context-dependent effects of ASXL1 mutation in myeloid disorders and provide insights into the mechanisms underlying neutrophil differentiation in ASXL1-mutant CNL.
Published in
Dual ASXL1 and CSF3R mutations drive myeloid-biased stem cell expansion and enhance neutrophil differentiation
Darmusey L, Bagley AJ, Nguyen TT et al. · Blood advances 2025 · PMID 39777477 · doi:10.1182/bloodadvances.2024014362
This dataset
Open GSE266087 in finder → Find more mouse ChIP / ATAC / CUT&Tag datasets →
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 GSE266087_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1105868 and SRA study SRP504575. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39777477) ↗
Study design
3 × sgNT/Empty vs 3 × sgB2/Empty vs 3 × sgNT/T618I vs 3 × sgB2/T618I

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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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