GEO series

Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling [ChIP-seq and CUT&Tag]

GSE239468 Mus musculus (mouse) ChIP-seq / ATAC-seq (genome binding and open chromatin) 46 samples Submitted 2024/04/14 Platform GPL30172

At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · mouse · 46 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: 46 samples: 46 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.
Paper: Condensate-Promoting ENL Mutation Drives Tumorigenesis In Vivo Through Dynamic Regulation of Histone Modifications and Gene ExpressionCancer discovery · 2024

Summary (written by the submitters)

Gain-of-function mutations in the chromatin ‘reader’ ENL, identified in AML and Wilms tumor, have been shown to induce aberrant formation of transcriptional condensates in cellular systems. However, the precise role of these mutations and their condensate forming property in tumorigenesis remains unclear. By creating a conditional knock-in mouse model for the most prevalent ENL mutation, we establish ENL mutant as a bona fide oncogenic driver of acute myeloid leukemia in vivo.

Read the full summary ↓

Heterozygous expression of ENL mutant perturbs the normal hematopoietic hierarchy and results in the aberrant expansion of myeloid progenitors with increased self-renewal property. Furthermore, the ENL mutant remodels histone modifications to alter differentiation processes and drive oncogenic gene expression during hematopoietic development. Importantly, targeted point mutagenesis to disrupt the condensate formation property completely abolishes ENL mutant’s oncogenic function in hematopoietic stem and progenitor cells (HSPCs). Lastly, short-term treatment with a small molecule inhibitor that blocks the acetyl-binding activity of ENL mutant reverts its impact on chromatin and significantly delays leukemia development in mice. Our studies reveal the crucial biological function of mutation-induced transcriptional condensates in chromatin regulation and cancer in vivo and provide proof-of-concept for targeting of pathogenic condensates as a promising therapy for certain cancers.

Published in

Condensate-Promoting ENL Mutation Drives Tumorigenesis In Vivo Through Dynamic Regulation of Histone Modifications and Gene Expression

Liu Y, Li Q, Song L et al. · Cancer discovery 2024 · PMID 38655899 · doi:10.1158/2159-8290.CD-23-0876

This dataset

Open GSE239468 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 GSE239468_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 PRJNA999348 and SRA study SRP451847. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 38655899) ↗

Study design

46 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 46 sample titles: 46 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

GSM7665650 LSK cells, Enl-WT, H3K27ac, CUT&Tag
GSM7665651 LSK cells, Enl-T1, H3K27ac, CUT&Tag
GSM7665652 GMP cells, Enl-WT, H3K27ac, CUT&Tag
GSM7665653 GMP cells, Enl-T1, H3K27ac, CUT&Tag
GSM7665654 L-GMP cells, Enl-WT, H3K27ac, CUT&Tag
GSM7665655 L-GMP cells, Enl-T1, H3K27ac, CUT&Tag
GSM7665656 cKit+Mac1+ cells, Enl-WT, H3K27ac, CUT&Tag
GSM7665657 cKit+Mac1+ cells, Enl-T1, H3K27ac, CUT&Tag
GSM7665658 cKit-Mac1+ cells, Enl-WT, H3K27ac, CUT&Tag
GSM7665659 cKit-Mac1+ cells, Enl-T1, H3K27ac, CUT&Tag
GSM7665660 LSK cells, Enl-WT, H3K27me3, CUT&Tag
GSM7665661 LSK cells, Enl-T1, H3K27me3, CUT&Tag
GSM7665662 GMP cells, Enl-WT, H3K27me3, CUT&Tag
GSM7665663 GMP cells, Enl-T1, H3K27me3, CUT&Tag
GSM7665664 L-GMP cells, Enl-WT, H3K27me3, CUT&Tag
GSM7665665 L-GMP cells, Enl-T1, H3K27me3, CUT&Tag
GSM7665666 cKit+Mac1+ cells, Enl-WT, H3K27me3, CUT&Tag
GSM7665667 cKit+Mac1+ cells, Enl-T1, H3K27me3, CUT&Tag
GSM7665668 cKit-Mac1+ cells, Enl-WT, H3K27me3, CUT&Tag
GSM7665669 cKit-Mac1+ cells, Enl-T1, H3K27me3, CUT&Tag
GSM7665670 LSK cells, Enl-T1, H3K27ac, TDI11055, CUT&Tag
GSM7665671 GMP cells, Enl-T1, H3K27ac, TDI11055, CUT&Tag
GSM7665672 GMP cells, Enl-WT, p300, ChIP-seq
GSM7665673 GMP cells, Enl-T1, p300, ChIP-seq
GSM7665674 L-GMP cells, Enl-WT, p300, ChIP-seq
GSM7665675 L-GMP cells, Enl-T1, p300, ChIP-seq
GSM7665676 GMP cells, Enl-WT, input, ChIP-seq
GSM8064098 L-GMP cells, Enl-WT, DMSO, 24h, H3K27ac, CUT&Tag
GSM8064099 L-GMP cells, Enl-T1, DMSO, 24h, H3K27ac, CUT&Tag
GSM8064100 L-GMP cells, Enl-T1, A485, 3h, H3K27ac, CUT&Tag
GSM8064101 L-GMP cells, Enl-T1, A485, 6h, H3K27ac, CUT&Tag
GSM8064102 L-GMP cells, Enl-T1, A485, 24h, H3K27ac, CUT&Tag
GSM8064103 LSK cells, Flag-Enl-WT, H3K27ac, CUT&Tag
GSM8064104 LSK cells, Flag-Enl-T1, H3K27ac, CUT&Tag
GSM8064105 LSK cells, Flag-Enl-T1-H116P, H3K27ac, CUT&Tag
GSM8064106 LSK cells, Flag-Enl-WT, Flag, CUT&Tag
GSM8064107 LSK cells, Flag-Enl-T1, Flag, CUT&Tag
GSM8064108 LSK cells, Flag-Enl-T1-H116P, Flag, CUT&Tag
GSM8064109 LSK cells, Flag-Enl-WT, DMSO, H3K27ac, CUT&Tag
GSM8064110 LSK cells, Flag-Enl-T1, DMSO, H3K27ac, CUT&Tag

+ 6 more — browse all 46 samples with per-sample file links →

Datasets on a similar topic

GSE239470 Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling 74 samples shares enl, condensate-promoting, tumorigenesis, remodeling, chromatin, mutation
GSE239469 Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling [RNA-seq] 28 samples shares enl, condensate-promoting, tumorigenesis, remodeling, chromatin, mutation
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, chip-seq
GSE274493 The remodeling of bivalent chromatin is essential for mouse peri-implantation embryogenesis [CUT&Tag] 46 samples shares cut, remodeling, chromatin
GSE304211 H4K16ac contributes to chromatin compartment reorganization during mitotic and meiotic transitions [CUTnTAG] 128 samples shares cut, chromatin
GSE303384 Mechanism of maintenance and establishment of repression by the Mtg16 tumor suppressor [CUT&RUN, ChIP-Seq] 92 samples shares cut, chip-seq
GSE298418 MeCP2 stabilizes the glucocorticoid system in active chromatin regions [CUT&Tag] 63 samples shares cut, chromatin
GSE274875 A mutant ASXL1-EHMT complex contributes to heterochromatin dysfunction in clonal hematopoiesis and chronic monomyelocytic leukemia [Cut & Run] 38 samples shares cut, chromatin

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.