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Establishing competence for trophectoderm specification in mouse embryos before the first lineage bifurcation

GSE284147 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2025/10/24 Platform GPL24247
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: 12 samples, each with a distinct title — no replicated groupsGroups 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)
How embryonic blastomeres transition from totipotency to differentiation remains a fundamental question in developmental biology. Here, we uncover the transcription factor CEBPa as an orchestrator of this process. CEBPa expression is first activated by NR5A2 at the 2-cell to 4-cell transition and in a second wave peaks in the trophectoderm of blastocysts.
Read the full summary ↓
Loss of CEBPa disrupts timely blastocyst formation and impairs trophectoderm development, while its forced expression in embryonic stem cells drives differentiation into trophectoderm-like cells. Mechanistically, CEBPa sequentially activates key trophectoderm enhancers in a dose-dependent manner. At the 4-cell stage, some of these trophectoderm enhancers are already active while others are primed or still closed, placing blastomeres in a state of alert. These findings establish CEBPa as a molecular switch that equips 4-cell blastomeres with the competence for trophectoderm differentiation, defining the earliest steps in cell fate bifurcation and shedding new light on the mechanisms driving embryonic lineage specification.
This dataset
Open GSE284147 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 GSE284147_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 PRJNA1197455 and SRA study SRP551184. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
12 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 12 sample titles: 12 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
Datasets on a similar topic

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

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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.