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Transcriptional profile of ER71 EYFP positive/negative cells in ER71 WT and MT embryos

ABSTRACT: ER71 mutant embryos are nonviable and lack hematopoietic and endothelial lineages. To further define the functional role for ER71 in cell lineage decisions, we generated genetically modified mouse models. We engineered an ER71-EYFP transgenic mouse model by fusing the 3.9 kb ER71 promoter to the EYFP reporter gene. Using FACS and transcriptional profiling, we examined the EYFP+ populations of cells in ER71 mutant and wildtype littermates. In the absence of ER71, we observed an increase in the number of EYFP expressing cells, increased expression of the cardiac molecular program and decreased expression of the hemato-endothelial program compared to the wildtype littermate controls. We have also generated a novel ER71-Cre transgenic mouse model using the same 3.9 kb ER71 promoter. Genetic fate mapping studies revealed that the ER71 expressing cells daughter hematopoietic and endothelial lineages in the wildtype background. In the absence of ER71, these cell populations contributed to alternative mesodermal lineages including the cardiac lineage. To extend these analyses, we used an inducible ES/EB system and observed that ER71 overexpression repressed cardiogenesis. Together, these studies identify ER71 as a critical regulator of mesodermal fate decisions, acting to specify the hematopoietic and endothelial lineages at the expense of cardiac lineages. This enhances our understanding of the mechanisms that govern mesodermal fate decisions early during embryogenesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE32223 | GEO | 2011/11/02

SECONDARY ACCESSION(S): PRJNA147215

REPOSITORIES: GEO

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Transcriptional profile of ER71 EYFP positive/negative cells in ER71 WT and MT embryos

Project description:ER71 mutant embryos are nonviable and lack hematopoietic and endothelial lineages. To further define the functional role for ER71 in cell lineage decisions, we generated genetically modified mouse models. We engineered an ER71-EYFP transgenic mouse model by fusing the 3.9 kb ER71 promoter to the EYFP reporter gene. Using FACS and transcriptional profiling, we examined the EYFP+ populations of cells in ER71 mutant and wildtype littermates. In the absence of ER71, we observed an increase in the number of EYFP expressing cells, increased expression of the cardiac molecular program and decreased expression of the hemato-endothelial program compared to the wildtype littermate controls. We have also generated a novel ER71-Cre transgenic mouse model using the same 3.9 kb ER71 promoter. Genetic fate mapping studies revealed that the ER71 expressing cells daughter hematopoietic and endothelial lineages in the wildtype background. In the absence of ER71, these cell populations contributed to alternative mesodermal lineages including the cardiac lineage. To extend these analyses, we used an inducible ES/EB system and observed that ER71 overexpression repressed cardiogenesis. Together, these studies identify ER71 as a critical regulator of mesodermal fate decisions, acting to specify the hematopoietic and endothelial lineages at the expense of cardiac lineages. This enhances our understanding of the mechanisms that govern mesodermal fate decisions early during embryogenesis. 12samples were analyzed, including triplicates of WT; EYFP positive, WT EYFP negative, ER71 MT; EYFP positive and ER71 MT; EYFP negative cells

2011-11-02 | E-GEOD-32223 | biostudies-arrayexpress

Expression data from day 3 Flk-1 mesoderm between ER71 overexpressed and ER71 knockout mouse embryonic stem cell

2012-02-20 | GSE35793 | GEO

Expression data from day 3 Flk-1 mesoderm between ER71 overexpressed and ER71 knockout mouse embryonic stem cell

Project description:Ets transcription factor ER71 is critical for Flk-1 mesoderm specification to different cell lineages. In this dataset, we determine to investigate the mechanisms by which ER71 regulates hematopoietic and endothelial cell versus cardiac cell lineage development. Expression of all four Flk-1+ mesoderm populations (i.e. Er71 overexpressed versus control, Er71 deficient versus control Flk-1+ mesoderm) was compared. Specifically, we sorted Flk-1+ mesoderm from day 3 differentiated embryonic stem(ES) cells, including induced Er71 and control ES cells, as well as Er71+/+ as well as Er71-/- ES cells .

2012-02-20 | E-GEOD-35793 | biostudies-arrayexpress

Genome-wide analysis of ETS factor ER71/ETV2 chromatin occupancy

Project description:We discover that ER71/ETV2 initiates hemangiogenic program by activating blood and endothelial cell lineage specifying genes while enhancing FLK1 expression and expanding hemangioblast population. Furthermore, ER71/ETV2 establishes an ETS hierarchy by directly activating Ets genes in hematopoietic and endothelial cell lineage development. As such, ER71/ETV2-initiated blood and endothelial cell program is maintained by ER71/ETV2 downstream ETS factors through an ETS switching mechanism.

2015-03-30 | GSE59402 | GEO

Genome-wide analysis of ETS factor ER71/ETV2 chromatin occupancy

2015-03-30 | E-GEOD-59402 | biostudies-arrayexpress

ER71/ETV2-mediated direct reprogramming of human dermal fibroblasts (HDFs) into endothelial-like cells

Project description:Samples 1-6: HDFs transduced with ER71/ETV2 were sorted on KDR expression at day 7. The isolated KDR+ cells together with human umbilical venous endothelial cells (HUVECs) and untransduced HDFs were subjected to genomic gene expression profiling. A significant number of genes related with vessel development and angiogenesis was significantly upregulated in KDR+ cells, compared to control HDFs. These findings strongly argue that ER71/ETV2 directly reprograms human fibroblasts to functional endothelial-like cells, which could be useful for disease investigation as well as autologous cell therapy. Samples 7-12: HDFs transduced with ER71/ETV2 were sorted on KDR expression at day 7. The isolated KDR+ cells were further cultured up to day 93. The further cultured cells together with human umbilical venous endothelial cells (HUVECs) and untransduced HDFs were subjected to genomic gene expression profiling. A significant number of genes related with vessel development and angiogenesis was significantly upregulated in the further cultured cells, compared to control HDFs. These findings strongly argue that ER71/ETV2 directly reprograms human fibroblasts to functional endothelial-like cells, which could be useful for disease investigation as well as autologous cell therapy.

2013-09-12 | GSE50801 | GEO

ER71/ETV2-mediated direct reprogramming of human dermal fibroblasts (HDFs) into endothelial-like cells

2013-09-12 | E-GEOD-50801 | biostudies-arrayexpress

ETV2/ER71 regulates hematovascular lineage generation and vascularization through an H3K9 demethylase, KDM4A

Project description:ETV2/ER71, an ETS transcription factor, is critical for hematopoiesis and vascular development. However, knowledge on the molecular mechanisms behind ETV2-mediated gene transcription is limited. Here, we show that ETV2 together with KDM4A, an H3K9 demethylase, regulates hematopoietic and endothelial genes. Etv2-/- mouse embryonic stem cells (mESCs), which fail to generate hematopoietic and endothelial cells, showed enhanced levels of H3K9me3 on hematopoietic and endothelial genes. ETV2 interacts with KDM4A and the ETV2-mediated transcriptional activation of hematopoietic and endothelial genes is dependent on KDM4A histone demethylase activity. ETV2 and KDM4A co-occupy the transcription regulatory regions of genes whose expression is directly regulated by ETV2. Mice lacking Kdm4a and Etv2 in endothelial cells (Cdh5Cre;Kdm4af/f;Etv2f/f) displayed a more severe defect in perfusion recovery and neovascularization compared with Cdh5Cre;Kdm4af/f, Cdh5Cre;Etv2f/f mice and controls. Collectively, we demonstrated that ETV2 interacts with KDM4A and that this interaction is critical for FLK1+ cell generation, differentiation into the downstream lineages, and vascular regeneration.

2024-12-10 | GSE251753 | GEO

Cardiac organoids reveal mechanisms of human cardiogenesis

Project description:Self-organisation and coordinated morphogenesis of multiple cardiac lineages is essential for the development and function of the heart1-3. However, the absence of a human in vitro model that mimics the basic lineage architecture of the heart hinders research into developmental mechanisms and congenital defects4. Here, we describe the establishment of a reliable, lineage-controlled and high-throughput cardiac organoid platform. We show that cardiac mesoderm derived from human pluripotent stem cells robustly self-organises and differentiates into cardiomyocytes forming a cavity. Co-differentiation of cardiomyocytes and endothelial cells from cardiac mesoderm within these structures is required to form a separate endothelial layer. As in vivo, the epicardium engulfs these cardiac organoids, migrates into the cardiomyocyte layer and differentiates. We use this model to demonstrate that cardiac cavity formation is controlled by a mesodermal WNT-BMP signalling axis. Disruption of one of the key BMP targets in cardiac mesoderm, the transcription factor HAND1, interferes with cavity formation, which is consistent with its role in early heart tube and left chamber development5. Thus, the cardiac organoid platform represents a powerful resource for the quantitative and mechanistic analysis of early human cardiogenesis and defects that are otherwise inaccessible. Beyond understanding congenital heart disease, cardiac organoids provide a foundation for future translational research into human cardiac disorders.

2021-05-18 | PXD018306 | Pride

Sox7 regulates lineage decisions in cardiovascular progenitor cells

Project description:Specification of the mesodermal lineages requires a complex set of morphogenetic events orchestrated by interconnected signaling pathways and gene regulatory networks. The transcription factor Sox7 has critical functions in differentiation of multiple mesodermal lineages, including cardiac, endothelial, and hematopoietic. Using a doxycycline-inducible mouse embryonic stem cell (mESC) line, we have previously shown that expression of Sox7 in cardiovascular progenitor cells promotes expansion of endothelial progenitor cells. Here, we show that the ability of Sox7 to promote endothelial cell fate occurs at the expense of the cardiac lineage. Using ChIP-Seq coupled with ATAC-Seq we identify downstream target genes of Sox7 in cardiovascular progenitor cells and, by integrating these data with transcriptomic analyses, we define Sox7-dependent gene programs specific to cardiac and endothelial progenitor cells. Further, we demonstrate a protein-protein interaction between SOX7 and GATA4 and provide evidence that Sox7 interferes with the transcriptional activity of Gata4 on cardiac genes. In addition, we show Sox7 modulates WNT and BMP signaling during cardiovascular differentiation. Our data represent the first genome-wide analysis of Sox7 function and reveal a critical role for Sox7 in regulating signaling pathways that affect cardiovascular progenitor cell differentiation.

2019-07-06 | GSE133899 | GEO

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