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Cancer-associated Histone H3 N-terminal arginine mutations disrupt PRC2 activity and impair differentiation [CUT&RUN]

GSE239636 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 60 samples Submitted 2024/04/29 Platform GPL21626
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 60 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
60 samples: 20 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.
Paper
Cancer-associated Histone H3 N-terminal arginine mutations disrupt PRC2 activity and impair differentiationNature communications · 2024
Summary (written by the submitters)
Dysregulated epigenetic states are a hallmark of cancer and often arise from genetic alterations in epigenetic regulators. This includes missense mutations in histones, which, together with associated DNA, form nucleosome core particles. However, the oncogenic mechanisms of most histone mutations are unknown. Here, we demonstrate that cancer-associated histone mutations at arginines in the histone H3 N-terminal tail disrupt repressive chromatin domains, alter gene regulation, and dysregulate differentiation.
Read the full summary ↓
We find that histone H3R2C and R26C mutants reduce transcriptionally repressive H3K27me3. While H3K27me3 depletion in cells expressing these mutants was exclusively observed on the minor fraction of histone tails harboring the mutations, the same mutants recurrently disrupted broad H3K27me3 domains in the chromatin context, including near developmentally regulated promoters. H3K27me3 loss led to de-repression of differentiation pathways, with concordant effects between H3R2 and H3R26 mutants despite different proximity to the PRC2 substrate, H3K27. Functionally, H3R26C-expressing mesenchymal progenitor cells and murine embryonic stem cell-derived teratomas demonstrated impaired differentiation. Collectively, these data show that cancer-associated H3 N-terminal arginine mutations reduce PRC2 activity and disrupt chromatin-dependent developmental functions, a cancer-relevant phenotype.
Published in
Cancer-associated Histone H3 N-terminal arginine mutations disrupt PRC2 activity and impair differentiation
Nacev BA, Dabas Y, Paul MR et al. · Nature communications 2024 · PMID 38886411 · doi:10.1038/s41467-024-49486-5
This dataset
Open GSE239636 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 GSE239636_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 PRJNA1000464 and SRA study SRP452455. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 38886411) ↗
Study design
20 conditions, mostly in triplicate
H3WT_IgG ×3 H3WT_antiHA ×3 H3WT_antiH3K4me3 ×3 H3WT_antiH3K27me3 ×3 H3R2C_IgG ×3 H3R2C_antiHA ×3 H3R2C_antiH3K4me3 ×3 H3R2C_antiH3K27me3 ×3 +12 more

Supports a between-group comparison across 60 samples.

How we read this: 20 replicated groups read from 60 sample titles; they account for 60 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

+ 20 more — browse all 60 samples with per-sample file links →

Datasets on a similar topic

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