GEO series

Role of Snord116 in pituitary growth hormone deficiency of Prader-Willi Syndrome

GSE333730 Mus musculus (mouse) RNA-seq (gene expression) 20 samples Submitted 2026/07/30 Platform GPL24247

At a glance

RNA-seq (gene expression) · mouse · 20 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: 20 samples: 5 × KO, W4, vs 5 × WT, P0, vs 5 × KO, P0, vs 4 × WT, W4,Groups 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)

Prader-Willi Syndrome (PWS) is a complex genetic disorder resulting from the deficiency of several maternally imprinted genes, including SNORD116, in the 15q11-q13 region. Loss of Snord116 in mice recapitulates some of the most salient clinical features of PWS, including growth hormone (GH) deficiency and hypogonadism. This study explored the impact of Snord116 deficiency on early postnatal pituitary development and growth in Snord116 KO mice.

Read the full summary ↓

Snord116 was found to be expressed in both anterior and posterior pituitary. Pituitary transcriptomes of Snord116 KO and wild-type (WT) mice at two developmental stages, postnatal day 0 (P0) and 4 weeks of age, were interrogated and related to ex vivo analyses of GH secretion in the pituitaries of 5-week-old mice. Significant differences in pituitary transcriptomes were detected between Snord116 KO and WT mice at 4 weeks of age but not at P0. The differentially expressed genes and affected molecular pathways play important roles in regulating embryonic and postnatal pituitary development. Our results suggested that PWS GH deficiency was mainly due to pituitary hypoplasia and decreased GH production but not to reduced GH secretory function per se, implicating Snord116 in the specific molecular/cellular pathways that account for impaired postnatal pituitary development and GH deficiency in PWS.

This dataset

Open GSE333730 in finder → Find more mouse RNA-seq 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 GSE333730_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: 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 PRJNA1472292 and SRA study SRP704711. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

5 × KO, W4, vs 5 × WT, P0, vs 5 × KO, P0, vs 4 × WT, W4,

Supports a between-group comparison across 19 samples.

How we read this: 4 replicated groups read from 20 sample titles; they account for 19 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

GSM9771886 WT, W4, rep1 WT, W4,
GSM9771887 WT, W4, rep2 WT, W4,
GSM9771888 KO, W4, rep1 KO, W4,
GSM9771889 WT, W, rep3
GSM9771890 WT, W4, rep4 WT, W4,
GSM9771891 KO, W4, rep2 KO, W4,
GSM9771892 KO, W4, rep3 KO, W4,
GSM9771893 KO, W4, rep4 KO, W4,
GSM9771894 KO, W4, rep5 KO, W4,
GSM9771895 WT, W4, rep5 WT, W4,
GSM9771896 WT, P0, rep1 WT, P0,
GSM9771897 WT, P0, rep2 WT, P0,
GSM9771898 WT, P0, rep3 WT, P0,
GSM9771899 WT, P0, rep4 WT, P0,
GSM9771900 WT, P0, rep5 WT, P0,
GSM9771901 KO, P0, rep1 KO, P0,
GSM9771902 KO, P0, rep2 KO, P0,
GSM9771903 KO, P0, rep3 KO, P0,
GSM9771904 KO, P0, rep4 KO, P0,
GSM9771905 KO, P0, rep5 KO, P0,

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