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HIF1 Counteracts FOXO1/Bim-associated Follicle Atresia in Mouse Ovaries by Promoting Bcl-XL Expression

GSE304305 Mus musculus (mouse) RNA-seq (gene expression) 10 samples Submitted 2026/06/11 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 10 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
10 samples: 6 × Sal vs 4 × NACGroups 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)
Background In mammalian ovaries, the majorities of developing follicles (up to 95% in human) undergo atresia. A considerable part of follicle atresia is initiated by granulosa cell (GCs) apoptosis. Our previous work identified hypoxia-inducible factors 1 (HIF1) pathway induced by follicle-stimulating hormone as a protective factor against atresia, yet the molecular mechanism of follicles’ “norm” death, and how HIF1 pathway protect follicles has not been fully delineated.
Read the full summary ↓
Methods We employed a single-follicle, multi-dimensional profiling strategy based on serial sectioning, to dissect the signaling logic underlying physiological follicle fate decisions. Results HIF1 and forkhead box protein O1 (FOXO1) pathway show complementary activation patterns in GCs of healthy versus atretic mouse follicles. In growing mouse follicles, HIF1 pathway activity is associated with increased reactive oxygen species (ROS)-related signals, likely through enhanced granulosa-cell metabolic activity. Under the physiological conditions, ROS-related signals appear to help maintain HIF1 pathway activity in mouse granulosa cells during follicle growth, and are not by themselves associated with follicle atresia. HIF1 pathway appears to promote Bcl-XL expression, which may counterbalance FOXO1-associated atretic pressure. Conclusion In mouse ovaries, follicular fate appears to be associated with the dynamic balance between the pro-survival HIF1/Bcl-XL axis and the pro-apoptotic FOXO1/Bim axis.
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 GSE304305_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 PRJNA1300324 and SRA study SRP605794. Searching any of these in the dataset finder brings you back here.

Study design
6 × Sal vs 4 × NAC

Supports a between-group comparison across 10 samples.

How we read this: 2 replicated groups read from 10 sample titles; they account for 10 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
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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.