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The tumour suppressor STAG2 cooperates with DREAM to maintain quiescence in the urothelium [CUT&Run]

GSE288725 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 17 samples Submitted 2026/02/03 Platform GPL34328
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 17 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
17 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.
Summary (written by the submitters)
The maintenance of quiescence is essential for tissue homeostasis. STAG2 is one of the few genes mutated in the normal urothelium of organ donors, with mutant cells undergoing positive selection 1. STAG2 is also a major tumour suppressor gene 2–4 and its inactivation is an early event in bladder carcinogenesis 1,3. However, the mechanisms through which STAG2, a cohesin component, disrupt urothelial homeostasis remain largely unknown.
Read the full summary ↓
Here, we show that, in normal murine urothelial cells, Stag2 inactivation disrupts differentiation programs, induces a transient cell cycle entry, and primes cells for clonal expansion under stress conditions. In addition, STAG2 loss in urothelial cells expressing mutant FGFR3 —the most important bladder cancer oncogene 5— enhances tumour formation. For the first time, we show that STAG2 co-operates with the transcriptional complex DREAM, a master regulator of quiescence 6,7, binding to common genomic sites, including genes involved in cell cycle control. STAG2 loss results in changes in the expression of DREAM targets, its composition and chromatin distribution, and in the rewiring of chromatin interactions involving DREAM binding motifs in genes critical for cell cycle entry. Our findings provide strong evidence that STAG2 loss leads to changes in 3D genome organization through a novel mechanism involving the DREAM complex, leading to the disruption of homeostatic quiescence and oncogenic sensitivity.
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 GSE288725_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 PRJNA1219156 and SRA study SRP561558. Searching any of these in the dataset finder brings you back here.

Samples in this study

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+ 17 more — browse all 17 samples with per-sample file links →

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