GEO series
Cell autonomous regional differences in oligodendrocyte precursor cell development and response to oncohistone H3.3 K27M [ChIP-Seq]
GSE310474
Mus musculus (mouse)
ChIP-seq / ATAC-seq (genome binding and open chromatin)
40 samples
Submitted 2026/05/22
Platform GPL24247
At a glance
ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 40 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
- 40 samples: 40 samples, each with a distinct title — no replicated groupsGroups 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)
Diffuse midline glioma (DMG) is an incurable tumor arising in brainstem and midline structures. Most DMGs harbor missense histone H3 mutations replacing lysine 27 with methionine (H3 K27M). The mechanisms underlying regional selectivity for H3 K27M mutations, which are found almost exclusively in DMG, are not well understood. Here, we use a conditional knock-in mouse model to probe the postnatal brain region-specific oncogenic effects of H3.3 K27M in embryonic GFAP+ neural stem cells.
Read the full summary ↓
We show that H3.3 K27M reduces oligodendrocyte differentiation in a region-specific manner and increases postnatal proliferation of distinct progenitor states by brain region in vivo, selectively expanding the oligodendrocyte-lineage in the ventral pons. Cellular morphology, marker expression, and transcriptomic analyses of primary region-specific mouse OPC cultures demonstrated cell-intrinsic differences in wild-type brainstem and forebrain OPC differentiation dynamics. H3.3 K27M drives cell-autonomous increase in brainstem-derived OPC proliferation and disrupts intrinsic region-specific transcriptional programs, delaying differentiation in forebrain-derived OPCs and restraining full maturation of brainstem-derived OPCs. H3.3 K27M-mediated changes include brainstem-selective upregulation of genes in Bmp, Wnt, and Notch pathways that are relevant in DMG pathogenesis. Our findings reveal that H3.3 K27M differentially disrupts cell-autonomous regional oligodendrocyte development, which may provide an opportunistic window for brainstem-selective gliomagenesis.
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 GSE310474_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 PRJNA1366412 and SRA study SRP646867. Searching any of these in the dataset finder brings you back here.
Study design
40 samples, each with a distinct title — no replicated groups
Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.
How we read this: Read from 40 sample titles: 40 distinct titles with little repetition. 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
- GSM9301935 K27M brainstem OPC culture 59, no differentiation, H3K27me3 ChIP
- GSM9301936 K27M brainstem OPC culture 59, no differentiation, Input for H3K27me3 ChIP
- GSM9301937 K27M brainstem OPC culture 59, no differentiation, H3K4me3 ChIP
- GSM9301938 K27M brainstem OPC culture 59, no differentiation, Input for H3K4me3 ChIP
- GSM9301939 Control brainstem OPC culture 59, no differentiation, H3K27me3 ChIP
- GSM9301940 Control brainstem OPC culture 59, no differentiation, Input for H3K27me3 ChIP
- GSM9301941 Control brainstem OPC culture 59, no differentiation, H3K4me3 ChIP
- GSM9301942 Control brainstem OPC culture 59, no differentiation, Input for H3K4me3 ChIP
- GSM9301943 K27M brainstem OPC culture 61, no differentiation, H3K27me3 ChIP
- GSM9301944 K27M brainstem OPC culture 61, no differentiation, Input for H3K27me3 ChIP
- GSM9301945 K27M brainstem OPC culture 61, no differentiation, H3K4me3 ChIP
- GSM9301946 K27M brainstem OPC culture 61, no differentiation, Input for H3K4me3 ChIP
- GSM9301947 Control brainstem OPC culture 61, no differentiation, H3K27me3 ChIP
- GSM9301948 Control brainstem OPC culture 61, no differentiation, Input for H3K27me3 ChIP
- GSM9301949 Control brainstem OPC culture 61, no differentiation, H3K4me3 ChIP
- GSM9301950 Control brainstem OPC culture 61, no differentiation, Input for H3K4me3 ChIP
- GSM9301951 K27M cortex OPC culture 59, no differentiation, H3K27me3 ChIP
- GSM9301952 K27M cortex OPC culture 59, no differentiation, Input for H3K27me3 ChIP
- GSM9301953 K27M cortex OPC culture 59, no differentiation, H3K4me3 ChIP
- GSM9301954 K27M cortex OPC culture 59, no differentiation, Input for H3K4me3 ChIP
- GSM9301955 Control cortex OPC culture 59, no differentiation, H3K27me3 ChIP
- GSM9301956 Control cortex OPC culture 59, no differentiation, Input for H3K27me3 ChIP
- GSM9301957 Control cortex OPC culture 59, no differentiation, H3K4me3 ChIP
- GSM9301958 Control cortex OPC culture 59, no differentiation, Input for H3K4me3 ChIP
- GSM9301959 K27M cortex OPC culture 60, no differentiation, H3K27me3 ChIP
- GSM9301960 K27M cortex OPC culture 60, no differentiation, Input for H3K27me3 ChIP
- GSM9301961 K27M cortex OPC culture 60, no differentiation, H3K4me3 ChIP
- GSM9301962 K27M cortex OPC culture 60, no differentiation, Input for H3K4me3 ChIP
- GSM9301963 Control cortex OPC culture 60, no differentiation, H3K27me3 ChIP
- GSM9301964 Control cortex OPC culture 60, no differentiation, Input for H3K27me3 ChIP
- GSM9301965 Control cortex OPC culture 60, no differentiation, H3K4me3 ChIP
- GSM9301966 Control cortex OPC culture 60, no differentiation, Input for H3K4me3 ChIP
- GSM9301967 K27M cortex OPC culture 61, no differentiation, H3K27me3 ChIP
- GSM9301968 K27M cortex OPC culture 61, no differentiation, Input for H3K27me3 ChIP
- GSM9301969 K27M cortex OPC culture 61, no differentiation, H3K4me3 ChIP
- GSM9301970 K27M cortex OPC culture 61, no differentiation, Input for H3K4me3 ChIP
- GSM9301971 Control cortex OPC culture 61, no differentiation, H3K27me3 ChIP
- GSM9301972 Control cortex OPC culture 61, no differentiation, Input for H3K27me3 ChIP
- GSM9301973 Control cortex OPC culture 61, no differentiation, H3K4me3 ChIP
- GSM9301974 Control cortex OPC culture 61, no differentiation, Input for H3K4me3 ChIP
Datasets on a similar topic
- GSE310482 Cell autonomous regional differences in oligodendrocyte precursor cell development and response to oncohistone H3.3 K27M 217 samples shares k27m, oligodendrocyte, differences, oncohistone, autonomous, precursor, regional
- GSE290816 Cell autonomous regional differences in oligodendrocyte precursor cell development and response to oncohistone H3.3 K27M [RNA-seq] 142 samples shares k27m, oligodendrocyte, differences, oncohistone, autonomous, precursor, regional
- GSE290817 Cell autonomous regional differences in oligodendrocyte precursor cell development and response to oncohistone H3.3 K27M [scRNA-seq] 22 samples shares k27m, oligodendrocyte, differences, oncohistone, autonomous, precursor, regional
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- GSE278811 EZHIP-mediated PRC2 inhibition is required to maintain H3K27me3-dependent imprinting post fertilization [ChIP-Seq] 77 samples shares k27m, chip-seq
- GSE287032 H3K27me3 and the PRC1-H2AK119ub pathway cooperatively maintain heterochromatin and transcriptional silencing after the loss of H3K9 methylation [ChIP-seq] 20 samples shares k27m, chip-seq
- GSE277547 A novel histone H3K27 reader, CBFA2T2, inhibits H3K27me3 demethylation and tumor growth by regulating metabolic genes and metabolite levels [ChIP-seq II] 19 samples shares k27m, chip-seq
- GSE330241 Long-term maintenance of H3K27me3 in postmitotic neurons is dispensable for gene expression regulation [ChIP-Seq] 16 samples shares k27m, chip-seq
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