GEO series

Chromatin Modification Abnormalities by CHD7 and KMT2C Loss Promote Medulloblastoma Progression [CUT&Tag]

GSE263360 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 36 samples Submitted 2025/03/30 Platform GPL21626

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 36 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: 36 samples: 12 conditions, mostly in triplicateGroups 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)

Medulloblastoma, a common malignant pediatric brain tumor that typically originating from the cerebellum, is characterized by mutations in chromatin modifiers, highlighting the significance of epigenomic abnormalities in their progression. To prove this significance, the development and use of animal models that closely recapitulate the disease have been highly effective.

Read the full summary ↓

However, due to substantial time and cost limitations of developing genetically engineered mouse models, a complete understanding of the oncogenic potential of chromatin modifiers’ mutations found in human medulloblastomas is still elusive. In this study, we address this by CRISPR-mediated gene editing platform to knock out chromatin modifiers mutated human in SHH-subgroup medulloblastoma as well as the Ptch1 gene in cerebellar granule neuron progenitors. We functionally screened molecules involved tumor formation, identifying CHD7 and KMT2C as tumor suppressor genes. Multi-layered omics analysis revealed that these molecules epigenetically regulate the expression of Neurod1 that encodes a transcription factor crucial for neuronal differentiation, through histone H3 modification. Mutations impairing these factors suppress Neurod1, accelerating tumor growth. Conversely, forced expression of Neurod1 inhibits proliferation and promotes differentiation, underscoring its role as a key regulator in medulloblastoma aggressiveness. These findings not only demonstrate converging epigenomic abnormalities in SHH-subgroup medulloblastoma but also hold significant potential for evaluating epigenetic drugs targeting medulloblastoma, advancing the development of novel treatments.

This dataset

Open GSE263360 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 GSE263360_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 PRJNA1096764 and SRA study SRP499990. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Study design

12 conditions, mostly in triplicate

NC H3K4me1 ×3 NC H3K4me3 ×3 NC H3K27ac ×3 NC H3K27me3 ×3 Kmt2c_KO H3K4me1 ×3 Kmt2c_KO H3K4me3 ×3 Kmt2c_KO H3K27ac ×3 Kmt2c_KO H3K27me3 ×3 +4 more

Supports a between-group comparison across 36 samples.

How we read this: 12 replicated groups read from 36 sample titles; they account for 36 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

GSM8190212 NC H3K4me1 rep1 NC H3K4me1
GSM8190213 NC H3K4me3 rep1 NC H3K4me3
GSM8190214 NC H3K27ac rep1 NC H3K27ac
GSM8190215 NC H3K27me3 rep1 NC H3K27me3
GSM8190216 NC H3K4me1 rep2 NC H3K4me1
GSM8190217 NC H3K4me3 rep2 NC H3K4me3
GSM8190218 NC H3K27ac rep2 NC H3K27ac
GSM8190219 NC H3K27me3 rep2 NC H3K27me3
GSM8190220 NC H3K4me1 rep3 NC H3K4me1
GSM8190221 NC H3K4me3 rep3 NC H3K4me3
GSM8190222 NC H3K27ac rep3 NC H3K27ac
GSM8190223 NC H3K27me3 rep3 NC H3K27me3
GSM8190224 Kmt2c_KO H3K4me1 rep1 Kmt2c_KO H3K4me1
GSM8190225 Kmt2c_KO H3K4me3 rep1 Kmt2c_KO H3K4me3
GSM8190226 Kmt2c_KO H3K27ac rep1 Kmt2c_KO H3K27ac
GSM8190227 Kmt2c_KO H3K27me3 rep1 Kmt2c_KO H3K27me3
GSM8190228 Kmt2c_KO H3K4me1 rep2 Kmt2c_KO H3K4me1
GSM8190229 Kmt2c_KO H3K4me3 rep2 Kmt2c_KO H3K4me3
GSM8190230 Kmt2c_KO H3K27ac rep2 Kmt2c_KO H3K27ac
GSM8190231 Kmt2c_KO H3K27me3 rep2 Kmt2c_KO H3K27me3
GSM8190232 Kmt2c_KO H3K4me1 rep3 Kmt2c_KO H3K4me1
GSM8190233 Kmt2c_KO H3K4me3 rep3 Kmt2c_KO H3K4me3
GSM8190234 Kmt2c_KO H3K27ac rep3 Kmt2c_KO H3K27ac
GSM8190235 Kmt2c_KO H3K27me3 rep3 Kmt2c_KO H3K27me3
GSM8190236 Chd7_KO H3K4me1 rep1 Chd7_KO H3K4me1
GSM8190237 Chd7_KO H3K4me3 rep1 Chd7_KO H3K4me3
GSM8190238 Chd7_KO H3K27ac rep1 Chd7_KO H3K27ac
GSM8190239 Chd7_KO H3K27me3 rep1 Chd7_KO H3K27me3
GSM8190240 Chd7_KO H3K4me1 rep2 Chd7_KO H3K4me1
GSM8190241 Chd7_KO H3K4me3 rep2 Chd7_KO H3K4me3
GSM8190242 Chd7_KO H3K27ac rep2 Chd7_KO H3K27ac
GSM8190243 Chd7_KO H3K27me3 rep2 Chd7_KO H3K27me3
GSM8190244 Chd7_KO H3K4me1 rep3 Chd7_KO H3K4me1
GSM8190245 Chd7_KO H3K4me3 rep3 Chd7_KO H3K4me3
GSM8190246 Chd7_KO H3K27ac rep3 Chd7_KO H3K27ac
GSM8190247 Chd7_KO H3K27me3 rep3 Chd7_KO H3K27me3

Datasets on a similar topic

GSE263359 Chromatin Modification Abnormalities by CHD7 and KMT2C Loss Promote Medulloblastoma Progression [ATAC-seq] 11 samples shares kmt2c, chd7, medulloblastoma, abnormalities, modification, progression, chromatin
GSE255571 Chromatin remodeler CHD7 regulates neurogenic gene expression via controlling chromatin accessibility and modifications of histone marks H3K27me3 and H3K4me3 [Mouse CUT&Tag] 10 samples shares chd7, cut, modification, chromatin
GSE325799 KMT2C and KMT2D amplify GRHL2-driven enhancer activation [CUT&Tag] 80 samples shares kmt2c, cut
GSE336091 KMT2C catalytic activity regulates enhancer H3K4me1 and synaptic gene expression in cortical excitatory neurons [CUT&Tag] 48 samples shares kmt2c, cut
GSE304211 H4K16ac contributes to chromatin compartment reorganization during mitotic and meiotic transitions [CUTnTAG] 128 samples shares cut, chromatin
GSE289642 Noncanonical PRC2 chromatin association reveals a key role of EZHIP in intergenerational epigenetic memory transition [ChIP-Seq, Cut & Run] 107 samples shares cut, chromatin
GSE298418 MeCP2 stabilizes the glucocorticoid system in active chromatin regions [CUT&Tag] 63 samples shares cut, chromatin
GSE274493 The remodeling of bivalent chromatin is essential for mouse peri-implantation embryogenesis [CUT&Tag] 46 samples shares cut, chromatin

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