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PI3K/AKT signalling regulates mouse Inner Cell Mass (ICM) progenitor specification [FLASH-seq]

GSE265767 Mus musculus (mouse) RNA-seq (gene expression) 26 samples Submitted 2024/10/25 Platform GPL30172
At a glance

RNA-seq (gene expression) · mouse · 26 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
26 samples
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
PI3K/AKT signaling controls ICM maturation and proper epiblast and primitive endoderm specification in miceDevelopmental cell · 2025
Summary (written by the submitters)
The inner cell mass (ICM) of early mouse embryos is specified into Epiblast (Epi) and primitive endoderm (PrE) lineages during blastocyst formation. The antagonistic transcription factors (TFs) NANOG and GATA6 in combination with FGF/ERK signaling are central actors in ICM fate choice. However, what initiates the specification of the bipotent ICM progenitor and whether other factors are involved in this process is not fully understood yet.
Read the full summary ↓
Here, we report the key role of PI3K in mouse ICM progenitors specification. Surprisingly, while the PI3K/AKT signaling pathway is known for almost two decades to participate to the maintenance of pluripotency in stem cells, no role for this pathway in ICM cell fate decisions has been reported so far. This is likely due to the dynamic and asynchronous nature of ICM specification combined with the pleiotropic and rapidly evolving functions mediated by PI3K/AKT. By limiting the perturbations of the pathway to a short time-window corresponding to the early phase of ICM specification, we unravelled a dual role of PI3K in ICM progenitor, being required on the one hand for the maintenance of pluripotency TFs and, on the other hand, for the competence to engage into PrE differentiation in response to FGF signaling. Thus, our work identifies PI3K as a novel critical regulator of ICM progenitor specification in the mouse embryo.
Published in
PI3K/AKT signaling controls ICM maturation and proper epiblast and primitive endoderm specification in mice
Geiselmann A, Micouin A, Vandormael-Pournin S et al. · Developmental cell 2025 · PMID 39461340 · doi:10.1016/j.devcel.2024.10.001
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 GSE265767_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: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1104168 and SRA study SRP503897. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 26 more — browse all 26 samples with per-sample file links →

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