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p300/CBP inhibition promotes apoptosis in mouse embryos by impairing H1K75ac-mediated DNA repair from the 4-cell to blastocyst stage

GSE337703 Mus musculus (mouse) Single-cell RNA-seq 8 samples Submitted 2026/07/08 Platform GPL30215
At a glance

Single-cell RNA-seq · mouse · 8 samples

What it is
Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart. Read from the summary: GEO's own type field only says 'expression profiling by sequencing', so confirm it in the paper.
Organism
Mus musculus (mouse)
Samples
8 samples: 4 × Control sample vs 4 × Treatment sampleGroups 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)
Defective pre-implantation embryonic development is a major cause of implantation failure and early embryonic arrest. p300/CBP is known to influence blastocyst formation; nevertheless, its molecular regulatory cascades mediating murine embryonic development from the 4-cell to blastocyst stage are poorly understood. Here, we show that pharmacological inhibition of p300/CBP markedly reduced morula and blastocyst rate, increased embryonic fragmentation, and disrupted markers of compaction, polarization, and first lineage segregation from the 4-cell to blastocyst stage.
Read the full summary ↓
Smart-seq2 analysis showed that differentially expressed genes were enriched in pathways related to apoptosis, cell-cycle regulation, DNA modification, and embryonic development. Consistently, immunofluorescence analyses showed that p300/CBP inhibition increased apoptosis, suppressed cell proliferation, and promoted DNA damage accumulation. Mechanistically, p300/CBP inhibition reduced histone H1 lysine 75 acetylation (H1K75ac), leading to impaired DNA repair and subsequent activation of p38 signaling, thereby triggering apoptosis. Collectively, our findings identify a p300/CBP-H1K75ac-DNA repair-p38 MAPK signaling axis that maintains genome integrity and developmental competence in mouse pre-implantation embryos.
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 GSE337703_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: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1490616 and SRA study SRP715598. Searching any of these in the dataset finder brings you back here.

Study design
4 × Control sample vs 4 × Treatment sample

Supports a between-group comparison across 8 samples.

How we read this: 2 replicated groups read from 8 sample titles; they account for 8 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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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.