Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Redistribution of PU.1 partner transcription factor RUNX1 binding secures cell survival during leukemogenesis

ABSTRACT: Redistribution of PU.1 partner transcription factor RUNX1 binding secures cell survival during leukemogenesis

PROVIDER: PRJNA1055042 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR27290600.fastq.gz	Fastqsanger.gz
	SRR27290601.fastq.gz	Fastqsanger.gz
	SRR27290602.fastq.gz	Fastqsanger.gz
	SRR27290603.fastq.gz	Fastqsanger.gz
	SRR27298714.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 120

Similar Datasets

Redistribution of PU.1 partner transcription factor RUNX1 binding secures cell survival during leukemogenesis

Project description:Transcription factors (TFs) orchestrating lineage-development often control genes required for cellular survival. However, it is not well understood how cells survive when such TFs are lost, for example in cancer. PU.1 is an essential TF for myeloid fate, and mice with downregulated PU.1 levels develop acute myeloid leukemia (AML). Combining a multi-omics approach with a functional genetic screen, we reveal that PU.1-downregulated cells fundamentally change their survival control from cytokine-driven pathways to overexpression of an autophagy-predominated stem cell gene program, for which we also find evidence in human AML. Control of this program involves redirected chromatin occupancy of the PU.1 partner TF Runx1 to a lineage-inappropriate binding site repertoire. Hence, genomic reallocation of TF binding upon loss of a partner TF can act as a pro-oncogenic failsafe mechanism by sustaining cell survival during leukemogenesis.

| S-SCDT-10_1038-S44318-024-00295-Y | biostudies-other

Redistribution of PU.1 partner transcription factor RUNX1 binding secures cell survival during leukemogenesis

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-11-15 | GSE251674 | GEO

The hematopoietic master transcription factor PU.1 requires its interaction with the SWI/SNF remodeler to access chromatin de novo

Project description:PU.1 is a prototype master transcription factor (TF) of hematopoietic cell differentiation with diverse roles in different lineages. Analysis of its genome-wide binding pattern across PU.1 expressing cell types revealed manifold cell type-specific binding patterns. They are not consistent with the epigenetic and chromatin constraints to PU.1 binding observed in vitro, suggesting that PU.1 requires auxiliary factors to access DNA in vivo. Using a model of transient mRNA expression we show that PU.1 induction leads to the extensive remodeling of chromatin, redistribution of partner transcription factors and rapid initiation of a myeloid gene expression program in heterologous cell types. By probing PU.1 mutants for defects in chromatin access and screening for PU.1 proximal proteins in vivo, we found that its N-terminal acidic domain was required for the recruitment of SWI/SNF remodeling complexes, de novo chromatin access and stable binding as well as the redistribution of partner TFs.

2019-11-20 | PXD013167 | Pride

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

Project description: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. 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.

2024-11-15 | GSE250630 | GEO

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

2024-11-15 | GSE250629 | GEO

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

2024-11-15 | GSE250622 | GEO

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

2024-11-15 | GSE251672 | GEO

Transcription factor reorganization at chromatin secures myeloid progenitor cell survival in PU.1 downregulated leukemia [RNAseq_Cell lines]

2024-11-15 | GSE250620 | GEO

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

2024-11-15 | GSE250619 | GEO

The hematopoietic master transcription factor PU.1 requires its interaction with the SWI/SNF remodeler to access chromatin de novo [RNA-seq]

Project description:PU.1 is a prototype master transcription factor (TF) of hematopoietic cell differentiation with diverse roles in different lineages. Analysis of its genome-wide binding pattern across PU.1 expressing cell types revealed manifold cell type-specific binding patterns. They are not consistent with the epigenetic and chromatin constraints to PU.1 binding observed in vitro, suggesting that PU.1 requires auxiliary factors to access DNA in vivo. Using a model of transient mRNA expression we show that PU.1 induction leads to the extensive remodeling of chromatin, redistribution of partner transcription factors, and rapid initiation of a myeloid gene expression program in heterologous cell types. By probing mutant PU.1 variants for defects in chromatin access and screening for PU.1 proximal proteins in vivo, we found that its N-terminal acidic domain was required for the recruitment of SWI/SNF remodeling complexes, de novo chromatin access and stable binding as well as the redistribution of partner TFs.

2019-11-17 | GSE128836 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data