GEO series

Polycomb erasers BAP1 and UTX are dispensable for rapid bivalent gene activation but essential for enhancer establishment [CUT&Tag]

GSE329243 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 16 samples Submitted 2026/04/29 Platform GPL34290

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 16 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: 16 samples: 16 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)

Polycomb group (PcG) proteins safeguard cell identity by maintaining target genes in a transcriptionally repressed state through depositing two histone marks, H2A lysine-119 ubiquitination (H2AK119ub1) and H3 lysine-27 trimethylation (H3K27me3). BAP1 and UTX are thought to erase these marks during transcription activation, but their exact roles remain unclear.

Read the full summary ↓

Here we observe a rapid loss of H2AK119ub1, followed by a reduction in H3K27me3 levels at promoters upon transcription induction, coinciding with a swift dissociation of PRCs. With an acute degradation system, we show that BAP1 and UTX are dispensable for transcription activation or the dissolution of PcG repressive marks. Instead, they promote enhancer establishment during cell fate transition independent of their eraser enzymatic activity. Therefore, our study provides novel mechanistic insights that the dissolution of PcG-marks is transcription-dependent while UTX and BAP1 primarily function as bridging factors to construct enhancers, rather than as erasers of PcG memory.

This dataset

Open GSE329243 in finder → Find more mouse ChIP / ATAC / CUT&Tag 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 GSE329243_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: Look for peak files (.bed, .narrowPeak) and signal tracks (.bigWig) among the supplementary files; the raw reads are on ENA.

Also filed as BioProject PRJNA1458198 and SRA study SRP695306. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

16 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 16 sample titles: 16 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

GSM9699923 BAP1, +IAA, MLL4, rep1, CUT&Tag
GSM9699924 BAP1, +IAA, MLL4, rep2, CUT&Tag
GSM9699925 BAP1, -IAA, MLL4, rep1, CUT&Tag
GSM9699926 BAP1, -IAA, MLL4, rep2, CUT&Tag
GSM9699927 BAP1, WT, MLL4, rep1, CUT&Tag
GSM9699928 BAP1, WT, MLL4, rep2, CUT&Tag
GSM9699929 BAP1, C91A, MLL4, rep1, CUT&Tag
GSM9699930 BAP1, C91A, MLL4, rep2, CUT&Tag
GSM9699931 UTX, +IAA, MLL4, rep1, CUT&Tag
GSM9699932 UTX, +IAA, MLL4, rep2, CUT&Tag
GSM9699933 UTX, -IAA, MLL4, rep1, CUT&Tag
GSM9699934 UTX, -IAA, MLL4, rep2, CUT&Tag
GSM9699935 UTX, WT, MLL4, rep1, CUT&Tag
GSM9699936 UTX, WT, MLL4, rep2, CUT&Tag
GSM9699937 UTX, dMT, MLL4, rep1, CUT&Tag
GSM9699938 UTX, dMT, MLL4, rep2, CUT&Tag

Datasets on a similar topic

GSE329244 Polycomb erasers BAP1 and UTX are dispensable for rapid bivalent gene activation but essential for enhancer establishment [ChIP-seq] 64 samples shares bap1, utx, establishment, dispensable, activation, essential, polycomb
GSE297309 SKP1A-mediated degradation of PRC2 triggers activation of Polycomb-silenced gene [CUT&Tag] 108 samples shares cut, activation, polycomb
GSE303384 Mechanism of maintenance and establishment of repression by the Mtg16 tumor suppressor [CUT&RUN, ChIP-Seq] 92 samples shares cut, establishment
GSE325799 KMT2C and KMT2D amplify GRHL2-driven enhancer activation [CUT&Tag] 80 samples shares cut, activation
GSE274493 The remodeling of bivalent chromatin is essential for mouse peri-implantation embryogenesis [CUT&Tag] 46 samples shares cut, essential
GSE298002 Stage-specific Epigenetic Priming Amplifies Gene Activation During Lineage Commitment [CUT&Run] 38 samples shares cut, activation
GSE279279 KDM6A facilitates Xist upregulation at the onset of X inactivation [CUT&Run] 14 samples shares cut, activation
GSE304211 H4K16ac contributes to chromatin compartment reorganization during mitotic and meiotic transitions [CUTnTAG] 128 samples shares cut

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