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GSE276857 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 39 samples Submitted 2025/06/13 Platform GPL24676
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 39 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
Homo sapiens (human)
Samples
39 samples: 39 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 essential role of the core histones (H2A, H2B, H3 and H4) in DNA packaging has been well understood for decades, but the function of the linker histone (H1) remains enigmatic. H1 compacts nucleosome arrays in vitro, but the multiple H1 subtypes and variants encoded in mammalian genomes (11 in both mice and humans) hamper genetic studies to determine H1 function in vivo.
Read the full summary ↓
Challenging the prevailing view that linker histones are a general feature of heterochromatin, here we show a critical requirement for linker histones in the function of Polycomb Repressive complex 2 (PRC2). Through a CRISPR/Cas9 genetic screen in a fluorescent reporter cell line responsive to PRC2 perturbation, we identified an essential requirement for the poorly characterised gene CRAMP1 in PRC2-mediated repression. CRAMP1 localises to the promoters of all expressed H1 genes where it acts as a positive transcriptional regulator. Ablation of CRAMP1 provides a unique tool to simultaneously deplete all linker histones, which results in selective decompaction of H3K27me3-marked loci and derepression of PRC2 target genes without concomitant loss of PRC2 occupancy or enzymatic activity. Strikingly, in contrast to the broad genomic distribution previously ascribed to H1, we find that linker histones selectively localise to genomic loci marked by H3K27me3 across diverse cell types and organisms. Altogether, our data demonstrate a prominent role for linker histones in epigenetic repression by PRC2.
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 GSE276857_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 PRJNA1159305 and SRA study SRP531883. Searching any of these in the dataset finder brings you back here.

Study design
39 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 39 sample titles: 39 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
Datasets on a similar topic

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