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TRIM37 interacts with TRIM28 to maintain primordial germ cell identity during migration

GSE289334 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 18 samples Submitted 2026/06/26 Platform GPL24247Platform GPL34290
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 18 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
18 samples: 7 conditions, mostly in triplicateGroups 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)
During embryo development, germ cells segregate from soma to ensure the genome transmission of a species. Although the repression of somatic programs in germline specification is well studied, the molecular mechanisms that protect primordial germ cell (PGC) fate thereafter remain poorly understood. Here, we show that the ubiquitin ligase TRIM37 suppresses the somatic programs during PGC migration.
Read the full summary ↓
Trim37 mutant embryos exhibit PGC developmental defects from embryonic day 9.5 (E9.5) and depletion at E12.5, with Trim37-deficient PGCs transdifferentiating into somatic cells. Mechanistically, TRIM37 interacts with TRIM28 through its MATH domain to repress somatic gene expression in the nucleus. Forcing TRIM37 out of the nucleus causes PGC depletion. Additionally, the K27-linked polyubiquitination of TRIM28 catalyzed by TRIM37 augments their interaction and promotes the nucleus location of TRIM37. The impairment of TRIM37 ubiquitin ligase activity and mutations in TRIM28 ubiquitination sites both hinder PGC development. Furthermore, TRIM37 deficiency disrupts the DNA binding of TRIM28, which is mostly guided by AP2γ, leading to enhanced chromatin accessibility and increased H3K27ac levels, resulting in the upregulation of somatic genes. Our results shed light on the TRIM37-mediated epigenetic suppression mechanisms controlling germ cell fate maintenance and are relevant for the infertility of Mulibrey nanism patients.
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 GSE289334_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1222434 and SRA study SRP563274. Searching any of these in the dataset finder brings you back here.

Study design
7 conditions, mostly in triplicate
H3K27ac-control ×3 H3K27ac-T37KO ×3 H3K9me3-control ×3 H3K9me3-T37KO ×3 TRIM28-control ×2 TRIM28-T37KO ×2 AP2gama-control ×2

Supports a between-group comparison across 18 samples.

How we read this: 7 replicated groups read from 18 sample titles; they account for 18 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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