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Cell-autonomous function of Runx1 transcriptionally regulates megakaryocytic maturation in mice

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE45374 | GEO | 2013/03/22

SECONDARY ACCESSION(S): PRJNA193573

REPOSITORIES: GEO

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Similar Datasets

Cell-autonomous function of Runx1 transcriptionally regulates megakaryocytic maturation in mice

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-03-22 | E-GEOD-45374 | biostudies-arrayexpress

Cell-autonomous function of Runx1 transcriptionally regulates mouse megakaryocytic maturation.

Project description:RUNX1 transcription factor (TF) is a key regulator of megakaryocytic development and when mutated is associated with familial platelet disorder and predisposition to acute myeloid leukemia (FPD-AML). We used mice lacking Runx1 specifically in megakaryocytes (MK) to characterized Runx1-mediated transcriptional program during advanced stages of MK differentiation. Gene expression and chromatin-immunoprecipitation-sequencing (ChIP-seq) of Runx1 and p300 identified functional Runx1 bound MK enhancers. Runx1/p300 co-bound regions showed significant enrichment in genes important for MK and platelet homeostasis. Runx1 occupied genomic regions were highly enriched in RUNX and ETS motifs and to a lesser extent in GATA motif. Megakaryocytic specificity of Runx1/P300 bound enhancers was validated by transfection mutagenesis and Runx1/P300 co-bound regions of two key megakaryocytic genes Nfe2 and Selp were tested by in vivo transgenesis. The data provides the first example of genome wide Runx1/p300 occupancy in maturating primary FL-MK, unravel the Runx1-regulated program controlling MK maturation in vivo and identify a subset of its bona fide regulated genes. It advances our understanding of the molecular events that upon RUNX1mutations in human lead to the predisposition to familial platelet disorders and FPD-AML.

| S-EPMC3662678 | biostudies-literature

Cell-autonomous function of Runx1 transcriptionally regulates megakaryocytic maturation in mice (expression)

Project description:RUNX1 transcription factor (TF) is a key regulator of megakaryocytic development and when mutated is associated with familial platelet disorder and predisposition to acute myeloid leukemia (FPD-AML). We used mice lacking Runx1 specifically in megakaryocytes (MKs) to characterize the Runx1-mediated transcriptional program during advanced stages of MK differentiation. Gene expression and chromatin-immunoprecipitation-sequencing (ChIP-seq) of Runx1 andÂ p300Â identified functional Runx1-bound MK enhancers. Runx1/p300 co-bound regions showed significant enrichment in genes important for MK and platelet homeostasis. Runx1-bound regions were highly enriched in RUNX and ETS motifs and to a lesser extent in GATA motif.Â The data providesÂ the first example of genome-wide Runx1/p300 occupancy in maturating FL-MK,Â unravels the Runx1-regulated program controlling MK maturationÂ in vivoÂ andÂ identifies itsÂ bona fideÂ regulated genes. It advances our understandingÂ of the molecular events that upon mutations in RUNX1 lead to theÂ predisposition to familial platelet disorders and FPD-AML. Gene expression profiles of mature megakaryocytes taken from fetal livers of megakaryocyte-specific Runx1 knockout mice, using Runx1F/F/Pf4-Cre mice versus control (WT) mice.

2013-03-22 | E-GEOD-45373 | biostudies-arrayexpress

Cell-autonomous function of Runx1 transcriptionally regulates megakaryocytic maturation in mice (ChIP-seq)

Project description:RUNX1 transcription factor (TF) is a key regulator of megakaryocytic development and when mutated is associated with familial platelet disorder and predisposition to acute myeloid leukemia (FPD-AML). We used mice lacking Runx1 specifically in megakaryocytes (MKs) to characterize the Runx1-mediated transcriptional program during advanced stages of MK differentiation. Gene expression and chromatin-immunoprecipitation-sequencing (ChIP-seq) of Runx1 andÂ p300Â identified functional Runx1-bound MK enhancers. Runx1/p300 co-bound regions showed significant enrichment in genes important for MK and platelet homeostasis. Runx1-bound regions were highly enriched in RUNX and ETS motifs and to a lesser extent in GATA motif.Â The data providesÂ the first example of genome-wide Runx1/p300 occupancy in maturating FL-MK,Â unravels the Runx1-regulated program controlling MK maturationÂ in vivoÂ andÂ identifies itsÂ bona fideÂ regulated genes. It advances our understandingÂ of the molecular events that upon mutations in RUNX1 lead to theÂ predisposition to familial platelet disorders and FPD-AML. Examination of RUNX1 and P300 binding in WT mouse megakaryoctye cells using ChIP-Seq. The supplementary 'GSE45372_PeakList.txt' file includes a list of regions identified as binding for P300 or RUNX1 or both.

2013-03-22 | E-GEOD-45372 | biostudies-arrayexpress

Cell-autonomous function of Runx1 transcriptionally regulates megakaryocytic maturation in mice (expression)

Project description:RUNX1 transcription factor (TF) is a key regulator of megakaryocytic development and when mutated is associated with familial platelet disorder and predisposition to acute myeloid leukemia (FPD-AML). We used mice lacking Runx1 specifically in megakaryocytes (MKs) to characterize the Runx1-mediated transcriptional program during advanced stages of MK differentiation. Gene expression and chromatin-immunoprecipitation-sequencing (ChIP-seq) of Runx1 and p300 identified functional Runx1-bound MK enhancers. Runx1/p300 co-bound regions showed significant enrichment in genes important for MK and platelet homeostasis. Runx1-bound regions were highly enriched in RUNX and ETS motifs and to a lesser extent in GATA motif. The data provides the first example of genome-wide Runx1/p300 occupancy in maturating FL-MK, unravels the Runx1-regulated program controlling MK maturation in vivo and identifies its bona fide regulated genes. It advances our understanding of the molecular events that upon mutations in RUNX1 lead to the predisposition to familial platelet disorders and FPD-AML.

2013-03-22 | GSE45373 | GEO

Cell-autonomous function of Runx1 transcriptionally regulates megakaryocytic maturation in mice (ChIP-seq)

Project description:RUNX1 transcription factor (TF) is a key regulator of megakaryocytic development and when mutated is associated with familial platelet disorder and predisposition to acute myeloid leukemia (FPD-AML). We used mice lacking Runx1 specifically in megakaryocytes (MKs) to characterize the Runx1-mediated transcriptional program during advanced stages of MK differentiation. Gene expression and chromatin-immunoprecipitation-sequencing (ChIP-seq) of Runx1 and p300 identified functional Runx1-bound MK enhancers. Runx1/p300 co-bound regions showed significant enrichment in genes important for MK and platelet homeostasis. Runx1-bound regions were highly enriched in RUNX and ETS motifs and to a lesser extent in GATA motif. The data provides the first example of genome-wide Runx1/p300 occupancy in maturating FL-MK, unravels the Runx1-regulated program controlling MK maturation in vivo and identifies its bona fide regulated genes. It advances our understanding of the molecular events that upon mutations in RUNX1 lead to the predisposition to familial platelet disorders and FPD-AML.

2013-03-22 | GSE45372 | GEO

Dynamic combinatorial interactions of RUNX1 and cooperating partners regulates megakaryocytic differentiation in cell line models

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

2011-01-10 | GSE24779 | GEO

Runx1 downregulates stem cell and megakaryocytic transcription programs that support niche interactions

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-07-01 | E-GEOD-81182 | biostudies-arrayexpress

Runx1 downregulates stem cell and megakaryocytic transcription programs that support niche interactions

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

2016-07-01 | GSE81182 | GEO