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Genetic and epigenetic regulation of Treg cell fitness by autism-related chromatin remodeler CHD8

GSE279810 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 18 samples Submitted 2024/12/11 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 18 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
18 samples: 7 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
Genetic and epigenetic regulation of Treg cell fitness by autism-related chromatin remodeler CHD8Cellular & molecular biology letters · 2025
Summary (written by the submitters)
Chromatin remodeler CHD8 defines a subtype of autism. Its role in regulatory T cells (Tregs) that maintain immune tolerance through suppressing CD4+ and CD8+ effector T cells remain unknown. In this study, we found that Treg-specific CHD8 deletion led to early, fatal inflammatory disorders, due to increased CD4+ and CD8+ effector T cells.
Read the full summary ↓
CHD8 deletion increased Treg plasticity as evidenced by elevated effector T cell cytokine expression in Tregs. CHIP-seq uncovered that CHD8 binding genes were enriched in PI3K-Akt-mTOR signaling and several other pathways. RNA-seq and ATAC-seq revealed that CHD8 deletion upregulated a number of pathways, notably mTORC1 signaling and its mediated glycolysis that have been reported to promote Treg plasticity. Integrating RNA-seq data with ATAC-seq and/or CHIP-seq data indicates that CHD8 regulates gene expression in either chromatin remodeling- and/or CHD8 binding-dependent or -independent manner. Collectively, our findings suggest that CHD8 plays an important role in maintaining Treg fitness via genetic and epigenetic mechanisms.
Published in
Genetic and epigenetic regulation of Treg cell fitness by autism-related chromatin remodeler CHD8
Yang JQ, Wang C, Nayak RC et al. · Cellular & molecular biology letters 2025 · PMID 40155813 · doi:10.1186/s11658-025-00711-z
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 GSE279810_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 PRJNA1174721 and SRA study SRP539361. Searching any of these in the dataset finder brings you back here.

Study design
7 conditions, mostly in duplicate
1G-CHD8 ×2 2G-CHD8 ×2 1G-IgG ×2 2G-IgG ×2 KO1 ×2 WT ×2 KO2 ×2 Guo-W1 ×1 +3 more

Supports a between-group comparison across 14 samples.

How we read this: 7 replicated groups read from 18 sample titles; they account for 14 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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