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The dose-dependent role of PU.1 in Myeloid differentiation [ChIP-Seq]

ABSTRACT: A doxycycline-inducible system was used to induce PU.1 expression in cultured myeloid cell lines. The parent cell line used was BN (Kamath et al., Leukemia 22:1214-1225, 2008).

ORGANISM(S): Mus musculus

PROVIDER: GSE79191 | GEO | 2017/02/14

SECONDARY ACCESSION(S): PRJNA315131

REPOSITORIES: GEO

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PU.1 promotes cell cycle exit in the murine myeloid lineage associated with down-regulation of E2F1

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The dose-dependent role of PU.1 in Myeloid differentiation [small RNA-Seq]

Project description:A doxycycline-inducible system was used to induce PU.1 expression in cultured myeloid cell lines. The parent cell line used was BN (Kamath et al., Leukemia 22:1214-1225, 2008). Induction of PU.1 expression was previously demonstrated to lead to cell cycle exit and decreased expression of cell cycle genes. The goal of this study is expression profiling of small RNAs in cells with reduced or elevated PU.1 expression.

2017-02-14 | GSE79192 | GEO

PU.1 promotes cell cycle exit in the murine myeloid lineage associated with down-regulation of E2F1

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Expression data from PU.1low URE-/- AML cell line after treatment with small molecule acting as PU.1 inhibitor

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2017-12-07 | GSE77651 | 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.

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PU.1 interactome mouse bone marrow derived dendritic cells

Project description:Mouse bone marrow derived dendritic cells were generated by culturing bone marrow cells at a density of 0.5x10E6 cells/ml in RPMI-1640 supplemented with 5% FCS, 1% Pen/Strep, 5microM 2-mercaptoethanol, 20ng/ml GM-CSF. At day 7 dendritic cells were stimulated or not with 500 ng/ml LPS, and collected at day 10. 2x10E8 cells were used to prepare whole cell extracts and to perform PU.1 immunoprecipitaion with PU.1 antibody (T-21 Santa Cruz). IgG was used as control.

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Identification of PU.1 target genes by expression profiling of PUER cells

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Project description:We used Affymetrix Mouse Promoter 1.0R arrays to analyse PU.1-dependent promoters in mouse macrophages Keywords: PU.1 ChIP versus IgG ChIP, ChIP-Chip

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