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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]

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: GSE128835 | 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.

2019-11-17 | GSE128834 | GEO

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.

2019-11-17 | GSE128833 | 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

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.

2018-03-14 | GSE110018 | GEO

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

2018-03-14 | GSE103953 | GEO

The SNF2 ATPase-independent function of the INO80 chromatin remodeler [ChIP-seq]

Project description:In the multi-subunit INO80 chromatin-remodeling complex, all the auxiliary subunits assemble on three distinct domains of the catalytic chromatin remodeler INO80, which are N-terminal domain, HSA domain, and ATPase domain. While the ATPase and HSA domains and the auxiliary subunits assembling on the domains are known to be responsible for ATP hydrolysis and chromatin remodeling, it is largely unknown how the auxiliary subunits assembling on the INO80 N-terminal domain regulate the chromatin status. We identify both conserved and non-conserved auxiliary subunits of the INO80 complex in Arabidopsis thaliana. All the auxiliary subunits assemble on the conserved N-terminal domain, HSA domain, and ATPase domain of INO80 in Arabidopsis. While the auxiliary subunits assembling on the INO80 ATPase domain are required for the ATPase-dependent function, the INO80 N-terminal domain and the auxiliary subunits assembling on the domain can regulate gene expression and development even when the ATPase domain is absent, suggesting that INO80 has an ATPase-independent role. Furthermore, we find that a subclass of the COMPASS histone H3K4 methyltransferase complexes assemble on the INO80 N-terminal domain in the INO80 complex and function together with the other auxiliary subunits assembling on the INO80 N-terminal domain, thereby facilitating the ATPase-independent function. This study suggests that the conserved chromatin remodeler INO80 has an ATPase-independent role and demonstrates that the auxiliary subunits assembling on the INO80 N-terminal domain are required for the ATPase-independent role.

2021-05-25 | GSE162374 | GEO

The SNF2 ATPase-independent function of the INO80 chromatin remodeler [RNA-seq]

2021-05-25 | GSE162373 | GEO

Kosiuk2015-Geometric analysis of the Goldbeter minimal model for the embryonic cell cycle

Project description:A minimal model describing the embryonic cell division cycle at the molecular level in eukaryotes is analyzed mathematically. It is known from numerical simulations that the corresponding three-dimensional system of ODEs has periodic solutions in certain parameter regimes. We prove the existence of a stable limit cycle and provide a detailed description on how the limit cycle is generated. The limit cycle corresponds to a relaxation oscillation of an auxiliary system, which is singularly perturbed and has the same orbits as the original model. The singular perturbation character of the auxiliary problem is caused by the occurrence of small Michaelis constants in the model. Essential pieces of the limit cycle of the auxiliary problem consist of segments of slow motion close to several branches of a two dimensional critical manifold which are connected by fast jumps. In addition, a new phenomenon of exchange of stability occurs at lines, where the branches of the two-dimensional critical manifold intersect. This novel type of relaxation oscillations is studied by combining standard results from geometric singular perturbation with several suitable blow-up transformations.

2020-04-24 | BIOMD0000000933 | BioModels

Nuclear actin structure regulates chromatin accessibility [ATAC-seq]

Project description:Polymerized B-actin may provide a structural basis for chromatin accessibility and actin transport into the nucleus can guide mesenchymal stem cell (MSC) differentiation. Using MSC, we show that using CK666 to inhibit Arp2/3 directed secondary actin branching results in decreased nuclear actin structure, and significantly alters chromatin access measured with ATACseq at 24 h. The ATAC-seq results due to CK666 are distinct from those caused by cytochalasin D (CytoD), which enhances nuclear actin structure. In addition, nuclear visualization shows Arp2/3 inhibition decreases pericentric H3K9me3 marks. CytoD, alternatively, induces redistribution of H3K27me3 marks centrally. Such alterations in chromatin landscape are consistent with differential gene expression associated with distinctive differentiation patterns. Further, knockdown of the non-enzymatic monomeric actin binding protein, Arp4, leads to extensive chromatin unpacking, but only a modest increase in transcription, indicating an active role for actin-Arp4 in transcription. These data indicate that dynamic actin remodeling can regulate chromatin interactions.

2024-04-12 | GSE242944 | GEO

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