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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE128836 | GEO | 2019/11/17

REPOSITORIES: GEO

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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

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

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

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The hematopoietic master transcription factor PU.1 requires its interaction with the SWI/SNF remodeler to access chromatin de novo [CTV1_TALL_HELP ChIP-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.

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

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

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PU.1 represses and activates gene expression in early T cells by redirection of transcription factor ensembles [RNA-Seq]

Project description:Transcription factors normally regulate gene expression through their action at sites where they bind to DNA. However, the balance of activating and repressive functions that a transcription factor can mediate is not completely understood. Here, we show that PU.1 regulates gene expression in early stages of T-cell development both by recruiting partner transcription factors to its own binding sites and by depleting them from the binding sites that they may prefer when PU.1 is absent. Importantly, the loss of partner factors Satb1 and Runx1 occurs primarily from sites where PU.1 itself does not establish any detectable local binding. Genes linked to sites of partner factor ‘theft’ are enriched for considerable subsets of the genes PU.1 represses both in a model cell-line system and in normal T-cell development. Thus, system-level competitive recruitment dynamics permit PU.1 to affect gene expression both through own target sites and through action at a distance.

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PU.1 represses and activates gene expression in early T cells by redirection of transcription factor ensembles [ChIP-Seq]

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

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.

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