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

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: GSE52577 | GEO | 2013/12/11

SECONDARY ACCESSION(S): PRJNA229405

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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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.

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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.

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Project description:PU.1 is an Ets family transcription factor that is essential for the differentiation of both myeloid and lymphoid cells. PU.1 is down-regulated in classical Hodgkin lymphoma cells via methylation of the PU.1 promoter. To evaluate whether down-regulation of PU.1 is essential for the growth of cHL cells, we generated L428 derived cell lines conditionally express PU.1 by tet-off system (designated L428tetPU.1). Conditonally expressed PU.1 by tetracycline removal induced complete growth arrest and apoptosis in L428 cells. To elucidate the mechanisms underlying cell cycle arrest and apoptosis induced by PU.1, we compared gene expression profiles of L428tetPU.1 cells 0, 1 and 3 days after PU.1 induction, by DNA microarray. We extracted total RNA from L428tetPU.1 cells 0, 1 and 3 days after PU.1 induction by tetracycline removal. We compared gene expression profiles of KL428tetPU.1 cells 0, 1 and 3 days after PU.1 induction using DNA microarray analysis. 4 independent experiments were performed with each RNA samples.

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