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Histone 3 lysine 36 methylation shapes an epigenetic landscape in intestinal stem cell to orchestrate lipid metabolism and prevent cell senescence [CUT&Tag]

GSE283727 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 12 samples Submitted 2026/06/30 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 12 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
12 samples: 2 × Nsd2-ISC-WT-H3K4me vs 2 × Nsd2-ISC-KO-H3K4me vs 2 × Setd2-ISC-KO-H3K4meGroups 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 self-renewal capacity and differentiation potential of intestinal stem cells (ISCs) decline with age, leading to a loss of homeostasis and increased susceptibility to intestinal diseases. Despite the established importance of lipid metabolism and epigenetic regulation in ISC function, the molecular mechanisms linking these processes to aging-associated ISC dysfunction remain elusive.
Read the full summary ↓
Here, we demonstrate that H3K36 methylation, caused by NSD2 or SETD2, is critical to ISC fate. We found that the deficiency of H3K36 methylation results in reduced ISC proliferation and differentiation, disturbs fatty acid metabolism, and induces ISC senescence. This loss leads to increased chromatin accessibility and enhancer activation, impairing the function of the SWI/SNF chromatin remodeling complex and affecting genes expression. Importantly, we find that metabolic intervention can rescue the decline in ISC numbers due to H3K36 methylation deficiency. Our findings reveal a critical role for H3K36 methylation in maintaining epigenetic landscape to orchestrate lipid metabolism and determine intestinal stem cell fate.
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 GSE283727_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 PRJNA1195097 and SRA study SRP549828. Searching any of these in the dataset finder brings you back here.

Study design
2 × Nsd2-ISC-WT-H3K4me vs 2 × Nsd2-ISC-KO-H3K4me vs 2 × Setd2-ISC-KO-H3K4me

Supports a between-group comparison across 6 samples.

How we read this: 3 replicated groups read from 12 sample titles; they account for 6 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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