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Transcription factor reorganization at chromatin secures myeloid progenitor cell survival in PU.1 downregulated leukemia [ChIP-seq]

GSE251672 Homo sapiens (human) ChIP-seq / ATAC-seq (genome binding and open chromatin) 20 samples Submitted 2024/11/15 Platform GPL30173
At a glance

ChIP-seq / ATAC-seq (genome binding and open chromatin) · human · 20 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
Homo sapiens (human)
Topic
Acute myeloid leukemiaThis series is part of our curated briefing on it.
Samples
20 samples: 20 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
Redistribution of PU.1 partner transcription factor RUNX1 binding secures cell survival during leukemogenesisThe EMBO journal · 2024
Summary (written by the submitters)
Transcription factors (TFs) orchestrating lineage-development also control genes required for cellular survival. One such TF is PU.1, which is essential for myeloid development. Mice with downregulated PU.1 levels develop fatal acute myeloid leukemia (AML). However, because PU.1 is required for expression of growth factor receptors and signaling molecules, it has been unclear how PU.1-downregulated progenitors survive long enough to acquire additional alterations promoting leukemic transformation.
Read the full summary ↓
Combining a multi-omics approach with a functional genetic screen, we reveal herein that growth of PU.1-downregulated progenitors is secured by shifting survival control from cytokine-dependency towards overactivation of an autophagy-predominated stem cell program. This shift (for which we also find evidence in human AML) is linked to redirected binding of the PU.1 partner TF RUNX1 to chromatin sites previously not co-bound by PU.1. Hence, partner TF reallocation at chromatin can induce autophagy as a cell-autonomous failsafe mechanism to rescue cells from survival deficits caused by TF loss. Such growth-compensatory effects should be taken into account when considering TF as targets in cancer therapy.
Published in
Redistribution of PU.1 partner transcription factor RUNX1 binding secures cell survival during leukemogenesis
Bender A, Boydere F, Jayavelu AK et al. · The EMBO journal 2024 · PMID 39543396 · doi:10.1038/s44318-024-00295-y
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 GSE251672_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 PRJNA1055046 and SRA study SRP479179. Searching any of these in the dataset finder brings you back here.

Study design
20 samples, each with a distinct title — no replicated groups

Supports a case/control comparison: 10 samples read as cases, 10 as controls.

How we read this: Read from 20 sample titles: 20 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
More Acute myeloid leukemia datasets

Search all human ChIP / ATAC / CUT&Tag datasets in GEO →

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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.