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Mechanism of maintenance and establishment of repression by the Mtg16 tumor suppressor [CUT&RUN, ChIP-Seq]

GSE303384 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 92 samples Submitted 2026/07/01 Platform GPL34328
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 92 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
92 samples: 92 samples, each with a distinct title — no replicated groupsGroups 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)
The MTG family of transcriptional corepressors are frequent targets of chromosomal translocations and deletions in cancer, yet the mechanisms underlying tumor suppression are unclear. We employed a chemical-genetic approach to investigate the molecular mechanism of Mtg16-mediated repression. Analysis of nascent transcription revealed that Mtg16 is required to repress hundreds of genes and enhancers, including the oncogenes Myb and Gfi1b.
Read the full summary ↓
Because Mtg16 tightly regulated its own transcription, this model yielded a rapid “on/off/on” switch for Mtg16, providing a unique opportunity to study maintenance and establishment of repression within the same system. Mtg16 directly opposed histone acetylation at regulated loci, but analysis of H3K27ac revealed that changes in this mark correlated better with Mtg16 itself than with transcriptional activity. Importantly, both the relationship between Mtg16 and Class I HDAC activity and Mtg16-mediated re-establishment of repression were dependent target transcription. We propose that Mtg16 acts as a transcription-sensitive damper at highly accessible loci.
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 GSE303384_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 PRJNA1294979 and SRA study SRP602782. Searching any of these in the dataset finder brings you back here.

Study design
92 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 92 sample titles: 92 distinct titles with little repetition. 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

+ 52 more — browse all 92 samples with per-sample file links →

Datasets on a similar topic

Search all mouse ChIP / ATAC / CUT&Tag datasets in GEO →

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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.