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SUMOylation orchestrates a metastable heterochromatin state on a MORC3-responsive element to silence IFNB1 at a distance [ChIP-seq]

GSE292571 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 116 samples Submitted 2025/07/17 Platform GPL30173Platform GPL21103Platform GPL30172
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 116 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
116 samples: 46 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
SUMO operates from a unique long tandem repeat to keep innate immunity in checkNucleic acids research · 2025
Summary (written by the submitters)
Despite the pleiotropic role of SUMOylation, this pathway mainly functions to repress innate immunity in myeloid cells. Inactivating SUMOylation triggers a potent basal type I interferon (IFN1) response, amplified and coupled with an inflammatory response upon stimulation. These findings transposed to pre-clinical models with the demonstration that SUMOylation inhibitors (SUMOi) activate antitumor immunity in an IFN1-dependent manner.
Read the full summary ↓
Yet, how SUMOylation represses immune signaling remains largely unknown. We identified murine MORC3, a critical transcriptional repressor of the IFNB1 gene, as the top SUMO2/3 substrate in myeloid cells. We show that, in human monocytes, SUMO functions to repress basal IFNB1 in cis through an atypical/repeated MORC3-regulated element (MRE) concentrating/homing multiple PU.1 binding motifs. Inhibiting SUMOylation induces a 3D genome reorganization centered on the MRE, which, in turn, acquires both insulator and PU.1-driven enhancer activities, together with loss of H3.3 and H3K9me3 repressive marks and increased PU-1 binding. Paradoxically, MORC3, that binds PU.1, is massively recruited, yet unable to repress the MRE. Finally, we show that both MORC3 ATPase cycle and SUMOylation are critical for full MORC3 repressive activity. Our study identifies an unconventional mechanism in which SUMO, in concert with MORC3, orchestrates a metastable H3.3/H3K9me3 heterochromatin state on a multi-PU.1 binding platform element to shutdown unscheduled myeloid-specific IFN1 response.
Published in
SUMO operates from a unique long tandem repeat to keep innate immunity in check
Goffeney A, Hendriks IA, Morel V et al. · Nucleic acids research 2025 · PMID 40744492 · doi:10.1093/nar/gkaf750
This dataset
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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 GSE292571_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 PRJNA1240230 and SRA study SRP572195. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40744492) ↗
Study design
46 conditions, mostly in duplicate
Serie4, BlaER1 WT Monocytes, DMSO, Input, ×4 Serie4, BlaER1 WT Monocytes, TAK, Input, ×4 Serie4, BlaER1 WT Monocytes, DMSO, ChIP MORC3, ×4 Serie4, BlaER1 WT Monocytes, TAK, ChIP MORC3, ×4 Serie5, BlaER1 WT Lymphocytes, Input, ×4 Serie5, BlaER1 WT Lymphocytes, ChIP MORC3, ×4 Serie1, RAW 264.7, Input, ×2 Serie1, RAW 264.7, 24h ML, Input, ×2 +50 more

Supports a between-group comparison across 104 samples.

How we read this: 46 replicated groups read from 116 sample titles; they account for 104 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

+ 76 more — browse all 116 samples with per-sample file links →

Datasets on a similar topic

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