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Crypt density and recruited enhancers underlie intestinal tumour initiation [ATAC-seq]

GSE241382 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 32 samples Submitted 2024/11/15 Platform GPL24247
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 32 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
32 samples: 9 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
Crypt density and recruited enhancers underlie intestinal tumour initiationNature · 2025
Summary (written by the submitters)
Oncogenic mutations that drive colorectal cancer can be present in healthy intestines for long periods without overt consequence. Mutation of Adenomatous polyposis coli (Apc), the most common initiating event in conventional adenomas, activates Wnt signaling, hence conferring fitness on mutant intestinal stem cells (ISCs). Apc mutations may occur in ISCs that arose by routine self-renewal or by dedifferentiation of their progeny.
Read the full summary ↓
Although ISCs of these different origins are fundamentally similar, it is unclear if both generate tumours equally well in uninjured intestines. Also unknown is whether cis-regulatory elements are substantively modulated upon Wnt hyperactivation or as a feature of subsequent tumours. Here, we show in two mouse models that adenomas are not an obligatory outcome of Apc deletion in either ISC source but require proximity of mutant intestinal crypts. Reduced crypt density abrogates, and aggregation of mutant colonic crypts augments, adenoma formation. Moreover, adenoma-resident ISCs open chromatin at thousands of enhancers that are inaccessible in Apc-null ISCs not associated with adenomas. These cis-elements explain adenoma-selective gene activity and persist, with little further expansion of the repertoire, as other oncogenic mutations accumulate. Thus, cooperativity between neighbouring mutant crypts and new accessibility at specific enhancers are key steps early in intestinal tumourigenesis.
Published in
Crypt density and recruited enhancers underlie intestinal tumour initiation
Gaynor L, Singh H, Tie G et al. · Nature 2025 · PMID 39778708 · doi:10.1038/s41586-024-08573-9
This dataset
Open GSE241382 in finder → Find more mouse ChIP / ATAC / CUT&Tag datasets →
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 GSE241382_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 PRJNA1007884 and SRA study SRP456261. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 39778708) ↗
Study design
9 conditions, mostly in duplicate
Sec-Cre_ApcNull_Ileum_ISC ×4 ISC-Cre_ApcNull_KrasG12D ×4 Organoid_AKPS ×3 ISC-Cre_ApcNull_Duod_ISC ×2 WT_Ileal_ISC ×2 ISC-Cre_LowDoseTam_ApcNull ×2 ISC-Cre_ApcNull_KrasG12D_P53Null ×2 Organoid_M36_WT ×2 +10 more

Supports a between-group comparison across 23 samples.

How we read this: 9 replicated groups read from 32 sample titles; they account for 23 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
Datasets on a similar topic

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