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Stage-specific Epigenetic Priming Amplifies Gene Activation During Lineage Commitment [RELACS]

GSE298005 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 54 samples Submitted 2025/11/28 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 54 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
54 samples: 18 conditions, mostly in triplicateGroups 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
Stage-specific epigenetic priming amplifies gene activation during lineage commitmentScience advances · 2026
Summary (written by the submitters)
Neural progenitor cells exhibit developmental plasticity, as they are able to commit to different developmental trajectories in response to external stimuli. How these decisions are stabilized at the molecular level remains a highly active area of research. One way to stably integrate external stimuli into cell fate decisions is through epigenetic marks.
Read the full summary ↓
H4K16ac represents a unique epigenetic mark, as it modulates chromatin compaction and is the only known active histone modification that is transmitted intergenerationally. The deposition of H4K16ac is mediated by the evolutionarily conserved MSL acetyltransferase complex (MSLc), via its catalytic subunit MOF, and mutations in its components have been linked to neurodevelopmental disorders. To dissect the role of the MSLc, we employed a multi-pronged strategy combining both chronic and acute depletion models. Deletion of the MSLc structural backbone Msl1 in vivo resulted in embryonic lethality by E10, and single-cell multi-omics analysis revealed a systemic disruption in lineage commitment within the neuroectoderm. To distinguish primary molecular functions from secondary developmental consequences, we complemented this with a rapid degradation system in vitro, coupled to directed differentiation into two distinct neural lineages. We found that the MSLc facilitates accessibility at regulatory elements in the early stages of lineage commitment during neurogenesis. We observe a significant decrease in enhancer-promoter contacts in a specific subset of neurodevelopmental genes. In the absence of MSLc this gene group fails to reach adequate gene expression levels upon differentiation, resulting in abnormal morphology. Intriguingly, MSLc loss later on during differentiation does not phenocopy this. Our work reveals MSLc-mediated gene priming as a crucial mechanism potentiating the transcriptional activation of neurodevelopmental gene programs. Our study describes a new mode of epigenetic regulation which cements initial cell fate decisions and provides molecular insights into MSLc-associated developmental disorders.
Published in
Stage-specific epigenetic priming amplifies gene activation during lineage commitment
Foertsch A, Hirsch N, Seyfferth J et al. · Science advances 2026 · PMID 41894493 · doi:10.1126/sciadv.adz8889
This dataset
Open GSE298005 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 GSE298005_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 PRJNA1267103 and SRA study SRP587380. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 41894493) ↗
Study design
18 conditions, mostly in triplicate
RELACS ChIP-Seq, NPC, ctrl, H3K27ac, ×3 RELACS ChIP-Seq, NPC, ctrl, H3K27me3, ×3 RELACS ChIP-Seq, NPC, ctrl, H3K4me1, ×3 RELACS ChIP-Seq, NPC, ctrl, H3K4me3, ×3 RELACS ChIP-Seq, NPC, ctrl, H3K9me3, ×3 RELACS ChIP-Seq, NPC, ctrl, Input, ×3 RELACS ChIP-Seq, NPC, 24h Auxin treated, H3K2… ×3 RELACS ChIP-Seq, NPC, 24h Auxin treated, H3K2… ×3 +11 more

Supports a case/control comparison: 27 samples read as cases, 27 as controls.

How we read this: 18 replicated groups read from 54 sample titles; they account for 53 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

+ 14 more — browse all 54 samples with per-sample file links →

Datasets on a similar topic

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.