Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA142737 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE25079: Epistasis analysis of Runx1 and Gata1 over HoxA3 in hemogenic endothelium GSE25080: Genes regulated by HoxA3 in endothelial and hematopoietic progenitors Refer to individual Series
2010-12-20 | E-GEOD-25096 | biostudies-arrayexpress
Project description:We observe that HoxA3 represses hematopoieis by the repression of several transcription factors including Runx1 and Gata1. Up regulation of either Runx1 or Gata1 in the presence of HoxA3 reverted the hematopoietic repression. We have performed full genome analysis to determine the molecular signature of hematopoietic development in response to upregulation of Runx1 and Gata1. Endothelial progenitors were sorted from HoxA3 induced EBs, transduced with either control vector (control), Runx1 vector or Gata1 vector. Cells were co-cultured on Op9 for 5 days: in the following conditions: Control, HoxA3 upregulation, HoxA3 + Runx1 upregulation, HoxA3 + Gata1 upregulation in triplicate. After 5 days of culture,transduced cells were sorted (5000 cells) and prepared for microarray.
2010-12-20 | E-GEOD-25079 | biostudies-arrayexpress
Project description:We observe that HoxA3 represses hematopoieis by the repression of several transcription factors including Runx1 and Gata1. Up regulation of either Runx1 or Gata1 in the presence of HoxA3 reverted the hematopoietic repression. We have performed full genome analysis to determine the molecular signature of hematopoietic development in response to upregulation of Runx1 and Gata1.
2010-12-20 | GSE25079 | GEO
Project description:The transcription factor RUNX1 is required in the embryo for formation of the adult hematopoietic system. Here we describe the seminal findings that led to the discovery of RUNX1 and of its critical role in blood cell formation in the embryo from hemogenic endothelium. We also present RNA-Seq data demonstrating that hemogenic endothelial cells in different anatomic sites, which produce hematopoietic progenitors with dissimilar differentiation potentials, are molecularly distinct. Hemogenic endothelial cells and non-hemogenic endothelial cells in the yolk sac are more closely related to each other than either are to hemogenic or non-hemogenic endothelial cells in the major arteries. Thus, a major driver of the different lineage potentials of the committed erythro-myeloid progenitors that emerge in the yolk sac, versus hematopoietic stem cells that originate in the major arteries, is likely to be the distinct molecular properties of the hemogenic endothelial cells from which they are derived. We use bioinformatics analyses to predict signaling pathways active in arterial hemogenic endothelium, several of which are functionally validated pathways including Notch, Wnt, and Hedgehog. We also use a novel bioinformatics approach to assemble transcriptional regulatory networks and predict transcription factors that may be specifically involved in hematopoietic cell formation from arterial hemogenic endothelium, which is the origin of the adult hematopoietic system.
2018-10-05 | GSE103813 | GEO
Project description:Cell fate decisions during hematopoiesis are governed by lineage-specific transcription factors, such as RUNX1, SCL/TAL1, FLI1 and C/EBP family members. In order to gain insight about how these transcription factors regulate the activation of hematopoietic genes during embryonic development, we measured the genome-wide dynamics of transcription factor assembly on their target genes during the RUNX1-dependent transition from hemogenic endothelium to hematopoietic progenitors. Using a RUNX1-/- embryonic stem cell differentiation model expressing an inducible RUNX1 gene, we show that in the absence of RUNX1, SCL/TAL1, FLI1 and C/EBP-beta prime hematopoietic genes and that this early priming is required for correct temporal expression of the myeloid master regulator PU.1 and its downstream targets. After induction, RUNX1 binds to numerous new sites, initiating a local increase of histone acetylation and rapid global alterations in the binding patterns of SCL/TAL1 and FLI1. The acquisition of hematopoietic fate controlled by RUNX1 therefore does not represent the establishment of a new regulatory layer on top of a pre-existing hemogenic endothelium program but instead entails global reorganization of lineage-specific transcription factor assemblies. Microarray expression data obtained from differentiating murine hematopoietic cells, 3 independent biological replicates (measured twice) from iRUNX1 culture -/+DOX induction
2013-02-11 | E-GEOD-39662 | biostudies-arrayexpress
Project description:Cell fate decisions during hematopoiesis are governed by lineage-specific transcription factors, such as RUNX1, SCL/TAL1, FLI1 and C/EBP family members. In order to gain insight about how these transcription factors regulate the activation of hematopoietic genes during embryonic development, we measured the genome-wide dynamics of transcription factor assembly on their target genes during the RUNX1-dependent transition from hemogenic endothelium to hematopoietic progenitors. Using a RUNX1-/- embryonic stem cell differentiation model expressing an inducible RUNX1 gene, we show that in the absence of RUNX1, SCL/TAL1, FLI1 and C/EBPM-NM-2 prime hematopoietic genes and that this early priming is required for correct temporal expression of the myeloid master regulator PU.1 and its downstream targets. After induction, RUNX1 binds to numerous new sites, initiating a local increase of histone acetylation and rapid global alterations in the binding patterns of SCL/TAL1 and FLI1. The acquisition of hematopoietic fate controlled by RUNX1 therefore does not represent the establishment of a new regulatory layer on top of a pre-existing hemogenic endothelium program but instead entails global reorganization of lineage-specific transcription factor assemblies. ChIPseq data from transcription factors Runx1, Fli-1, Scl/Tal1 and C/EBPM-NM-2, histone modification H3K9Ac as well as RNA Pol II obtained from differentiating murine hematopoietic cells
2012-10-18 | E-GEOD-40235 | biostudies-arrayexpress
Project description:The differentiation of human embryonic stem cells to hematopoietic lineages initiates with the specification of hemogenic endothelium, a transient specialized endothelial precursor of all blood cells.Unfortunately, absence of hemogenic endothelium-specific markers as well as lack of consensus in the timing of hemogenic potential analysis and methodologies used to study the hematopoietic potential of this precursor prevents reaching clear and definite conclusions. Here, we demonstrate that the hemogenic potential of the endothelium precursor population sharply decline over the course of the differentiation process. Poly(A) RNA-sequencing on CD31+CD144+ population at day 6, day 8 and day 10 of EB diffferentiation with or without the addition of cytokines. Comparasion with hematopoietic committed population CD31+CD144- from day 10 of EB differentiation.
2018-10-25 | GSE109648 | GEO
Project description:Cell fate decisions during hematopoiesis are governed by lineage-specific transcription factors, such as RUNX1, SCL/TAL1, FLI1 and C/EBP family members. In order to gain insight about how these transcription factors regulate the activation of hematopoietic genes during embryonic development, we measured the genome-wide dynamics of transcription factor assembly on their target genes during the RUNX1-dependent transition from hemogenic endothelium to hematopoietic progenitors. Using a RUNX1-/- embryonic stem cell differentiation model expressing an inducible RUNX1 gene, we show that in the absence of RUNX1, SCL/TAL1, FLI1 and C/EBPβ prime hematopoietic genes and that this early priming is required for correct temporal expression of the myeloid master regulator PU.1 and its downstream targets. After induction, RUNX1 binds to numerous new sites, initiating a local increase of histone acetylation and rapid global alterations in the binding patterns of SCL/TAL1 and FLI1. The acquisition of hematopoietic fate controlled by RUNX1 therefore does not represent the establishment of a new regulatory layer on top of a pre-existing hemogenic endothelium program but instead entails global reorganization of lineage-specific transcription factor assemblies.
2012-10-18 | GSE40235 | GEO
Project description:Cell fate decisions during hematopoiesis are governed by lineage-specific transcription factors, such as RUNX1, SCL/TAL1, FLI1 and C/EBP family members. In order to gain insight about how these transcription factors regulate the activation of hematopoietic genes during embryonic development, we measured the genome-wide dynamics of transcription factor assembly on their target genes during the RUNX1-dependent transition from hemogenic endothelium to hematopoietic progenitors. Using a RUNX1-/- embryonic stem cell differentiation model expressing an inducible RUNX1 gene, we show that in the absence of RUNX1, SCL/TAL1, FLI1 and C/EBP-beta prime hematopoietic genes and that this early priming is required for correct temporal expression of the myeloid master regulator PU.1 and its downstream targets. After induction, RUNX1 binds to numerous new sites, initiating a local increase of histone acetylation and rapid global alterations in the binding patterns of SCL/TAL1 and FLI1. The acquisition of hematopoietic fate controlled by RUNX1 therefore does not represent the establishment of a new regulatory layer on top of a pre-existing hemogenic endothelium program but instead entails global reorganization of lineage-specific transcription factor assemblies.
2013-02-11 | GSE39662 | GEO