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Cohesin complex cooperates with PU.1 at super-enhancers to regulate the differentiation and identity of conventional dendritic cells

GSE326309 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 34 samples Submitted 2026/03/30 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 34 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
34 samples: 17 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.
Summary (written by the submitters)
Dendritic cell (DC) network consists of two major subsets- conventional (cDC) and plasmacytoid (pDC). cDCs undergo chromatin reorganization during their differentiation from hematopoietic progenitors to establish cDC-specific gene expression program. However, the requirement of architectural protein complex Cohesin in the differentiation of cDCs is poorly understood.
Read the full summary ↓
Herein we report that ablation of SMC3 or STAG2 subunits of Cohesin complex in DC-restricted progenitors leads to decrease in cDC, and increase in pDC compartment size. Cohesin complex controlled the functions of cDCs, such as antigen presentation and the expression of co-stimulatory molecules. The ablation of Cohesin complex repressed the expression of cDC identity genes and de-repressed the pDC-specific transcriptional signature in cDCs and pre-DCs. Mechanistically, Cohesin complex promoted the binding of PU.1, an ETS family transcription factor, at super-enhancers and supported chromatin loops favouring cDC differentiation. Notably, Cohesin-deficient DCs disturbed the steady-state haematopoiesis leading to myeloid hyperplasia. Our results reveal a transcriptional node involving Cohesin complex, PU.1 and super-enhancers in the regulation of lineage-specific gene expression program in cDCs.
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 GSE326309_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 PRJNA1445099 and SRA study SRP687697. Searching any of these in the dataset finder brings you back here.

Study design
17 conditions, mostly in duplicate
cDC_WT ×2 cDC_KO ×2 pDC_WT ×2 pDC_KO ×2 preDC_WT ×2 preDC_KO ×2 SMC1A_cDC_WT ×2 SMC1A_cDC_KO ×2 +9 more

Supports a between-group comparison across 34 samples.

How we read this: 17 replicated groups read from 34 sample titles; they account for 34 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
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