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SMAD1/5-Mediated Recruitment of the Histone Demethylase KDM1A Controls Cell Fate Programs in Embryonic Stem Cells [ChIP-seq]

GSE268911 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 18 samples Submitted 2025/08/15 Platform GPL16331
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: 8 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
SMAD1/5-mediated recruitment of the histone demethylase KDM1A controls cell fate programs in embryonic stem cellsThe Journal of biological chemistry · 2025
Summary (written by the submitters)
Bone morphogenetic proteins (BMPs) play diverse roles in mouse embryonic stem cell (mESC) biology. Recent studies suggest that BMPs induce multiple cell fates and enhance mESC heterogeneity by cross-activating multiple signaling pathways. Although BMPs primarily signal through SMAD1 and SMAD5 in mESCs, their roles remain incompletely defined.
Read the full summary ↓
Here, we investigated the SMAD signaling pathway using Smad1/5 double knockout (S1/5 dKO) mESCs. While SMAD1/5 depletion may influence mESC heterogeneity, single-cell RNA sequencing (scRNA-seq) revealed only minor differences between S1/5 dKO and WT cells, suggesting that the observed changes are not because of altered cell states. Chromatin immunoprecipitation sequencing (ChIP-seq) demonstrated that SMAD1/5 recruit the histone demethylase KDM1A/LSD1 to specific genomic regions, where it removes H3K4me1/2 marks associated with enhancers. Published scRNA-seq data from Kdm1a-deficient mESCs during embryoid body differentiation further supported this mechanism. This study reveals a transcriptional repression mechanism of SMAD1/5, involving KDM1A-dependent H3K4me1/2 depletion and the regulation of cell type–specific gene expression programs.
Published in
SMAD1/5-mediated recruitment of the histone demethylase KDM1A controls cell fate programs in embryonic stem cells
Morikawa M, Koinuma D, Sakai H et al. · The Journal of biological chemistry 2025 · PMID 40812426 · doi:10.1016/j.jbc.2025.110591
This dataset
Open GSE268911 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 GSE268911_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 PRJNA1119452 and SRA study SRP511387. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40812426) ↗
Study design
8 conditions, mostly in duplicate
wild-type mESCs, H3K4me1 ChIP-seq, ×2 Smad1/5 dKO mESCs, H3K4me1 ChIP-seq, ×2 wild-type mESCs, H3K4me2 ChIP-seq, ×2 Smad1/5 dKO mESCs, H3K4me2 ChIP-seq, ×2 wild-type mESCs, H3K9me2 ChIP-seq, ×2 Smad1/5 dKO mESCs, H3K9me2 ChIP-seq, ×2 wild-type mESCs, KDM1A ChIP-seq, ×2 Smad1/5 dKO mESCs, KDM1A ChIP-seq, ×2 +2 more

Supports a between-group comparison across 16 samples.

How we read this: 8 replicated groups read from 18 sample titles; they account for 16 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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