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SKP1A-mediated degradation of PRC2 triggers activation of Polycomb-silenced gene [ChIP-seq 2]

GSE297094 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 73 samples Submitted 2025/08/25 Platform GPL19057Platform GPL24247Platform GPL18480
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 73 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
73 samples: 32 conditions, mostly in duplicateGroups 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.
Paper
SKP1A bound to Polycomb-silenced genes mediates degradation of PRC2 and preconditions their activationMolecular cell · 2025
Summary (written by the submitters)
Polycomb group (PcG) proteins are evolutionarily conserved repressors of developmental genes. Paradoxically, the same PcG proteins also play roles in gene activation via mechanisms that are not yet fully understood. Here, we found that S-phase kinase-associated protein 1A (SKP1A), an essential factor of SCF (SKP1A/CULLIN1/F-box) ubiquitin ligases and a subunit of the PCGF1 (Polycomb group RING finger protein 1) component of Polycomb repressive complex 1 (PCGF1-PRC1), mediates the link between PcG-dependent gene regulation and ubiquitin-dependent proteasomal degradation.
Read the full summary ↓
By using differentiating mouse embryonic stem cells, we found that SKP1A removes EED, a core component of Polycomb repressive complex 2 (PRC2) that is bound to PcG target gene promoters, via proteasomal degradation, and it thereby sensitises these genes for subsequent activation. Furthermore, we show that SKP1A removes EED from the Meis2 promoter in the midbrain of developing mouse embryos, leading to Meis2 gene expression. In summary, we reveal here a previously unknown role of SKP1A in activating PcG-target genes via the proteasomal degradation of PRC2. This implies that SKP1A-containing PCGF1-PRC1 may confer reversibility on PcG-mediated gene silencing for robust spatiotemporal regulation of target genes.
Published in
SKP1A bound to Polycomb-silenced genes mediates degradation of PRC2 and preconditions their activation
Kondo T, Ito S, Takano J et al. · Molecular cell 2025 · PMID 40858113 · doi:10.1016/j.molcel.2025.08.004
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 GSE297094_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 PRJNA1262507 and SRA study SRP585002. Searching any of these in the dataset finder brings you back here.

Study design
32 conditions, mostly in duplicate
ChIP_SKP1A fl/fl ESC_EED_lot ×4 ChIP_SKP1A KO ESC_EED_lot ×4 ChIP_SKP1A fl/fl ESC_RING1B_lot ×4 ChIP_SKP1A KO ESC_RING1B_lot ×4 ChIP_EED KO ESC_FLAG_lot ×2 ChIP_EED KO+FLAG-EED WT ESC_FLAG_lot ×2 ChIP_EED KO+FLAG-EED 1-106KR ESC_FLAG_lot ×2 ChIP_EED KO+FLAG-EED 106-S KR ESC_FLAG_lot ×2 +25 more

Supports a between-group comparison across 72 samples.

How we read this: 32 replicated groups read from 73 sample titles; they account for 72 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

+ 33 more — browse all 73 samples with per-sample file links →

Datasets on a similar topic

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