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Pioneer factor ETV2 safeguards endothelial cell specification

ABSTRACT: Mechanisms of cell fate specification are central to developmental biology and regenerative medicine. ETV2 is a master regulator for the endothelial cell lineage specification. Here, we study mechanisms by which ETV2 overexpression in human iPSC-derived mesodermal progenitors efficiently specifies ECs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE267565 | GEO | 2025/04/01

REPOSITORIES: GEO

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Pioneer factor ETV2 safeguards endothelial cell specification

Project description:Pioneer factor ETV2 safeguards endothelial cell specification

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ETV2 upregulation marks the specification of early cardiomyocytes and endothelial cells during co-differentiation

Project description:The ability to differentiate human induced pluripotent stem cells (hiPSCs) efficiently into defined cardiac lineages, such as cardiomyocytes and cardiac endothelial cells, is crucial to study human heart development and model cardiovascular diseases in vitro. The mechanisms underlying the specification of these cell types during human development are not well-understood which limits fine-tuning and broader application of cardiac model systems. Here, we used the expression of ETV2, a master regulator of hematoendothelial specification in mice, to identify functionally distinct subpopulations during the co-differentiation of endothelial cells and cardiomyocytes from hiPSCs. Targeted analysis of single-cell RNA sequencing data revealed differential ETV2 dynamics in the two lineages. A newly created fluorescent reporter line allowed us to identify early lineage-predisposed states and show that a transient ETV2-high state initiates the specification of endothelial cells. We further demonstrated, unexpectedly, that functional cardiomyocytes can originate from progenitors expressing ETV2 at a low level. Our study thus sheds light on the in vitro differentiation dynamics of two important cardiac lineages.

2023-01-20 | GSE202901 | GEO

ETV2 Upregulation Marks the Specification of Early Cardiomyocytes and Endothelial Cells During Co-differentiation

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ETV2 cooperates with SCL for timely gene activation during hemogenic endothelium specification [RNA-Seq]

Project description:By RNA sequencing, we report here some hemato-vascular genes could be induced and some mesodermal/ cardiac genes could be repressed by SCL with delay in ES cell derived day 4.75 endothelial cells in the absence of ETV2

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Etv2-mediated hemangiogenic fate commitment of mesoderm

Project description:A comprehensive understanding of a lineage map and molecular mechanisms underlying lineage specification is fundamental to development. To this end, ETS transcription factor Etv2 functions as the master regulator of hematopoietic and endothelial cell formation. As such, Etv2 regulated hemangiogenesis provides an excellent model for assessing cell lineage specification. Herein, we generated several reporter embryonic stem (ES) cell lines to map developmental route pertaining to hemangiogenesis. We performed transcriptome analysis and high throughput CRISPR screening to further delineate molecular mechanisms regulating hemangiogenic lineage specification. We show a distinct lineage map of hemangiogenesis, in which hemangiogenic fate is specified not simply by the onset of Etv2 expression, but in a threshold-dependent manner. Importantly, VEGF-FLK1 signaling is necessary for efficiently achieving ETV2-threshold. Moreover, we find forkhead transcription factor Foxh1 to be required for FLK1 mesoderm formation. These studies provide a roadmap in hematopoietic and vascular cell generation and applications in regenerative medicine.

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Comparison of Flk-1+/Etv2- vs Flk-1+/Etv2+ populations

Project description:Screening for genes up in Etv2+ cells within Flk-1+ ES derived mesoderm Microarray analysis performed to screen for the candidate genes regulated by Etv2. Differentiated Flk-1+ mesoderm can be devided into Etv2+ or-. Etv2+ cells are assumed to be committed to hemato/endothelial cells. Comparison of two populations can reveal genes relevant in this commitment. Extract RNA from sorted Flk-1+/Etv2- vs Flk-1+/Etv2+ populations.Etv2-Venus KI ES cells were differentiated on OP9 for 4-5 days and Flk-1+ population was separated into Etv2-Venus+ or- cells. Total RNA was purified from each population for analysis.

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ETV2 primes hematoendothelial gene enhancers prior to hematoendothelial fate commitment

Project description:The lineage-determining transcription factor ETV2 is necessary and sufficient for hematoendothelial fate commitment. We investigated how ETV2-driven gene regulatory networks promote hematoendothelial fate commitment. We resolved the sequential determination steps of hematoendothelial versus cardiac differentiation from mouse embryonic stem cells. Etv2 was strongly induced and bound to the enhancers of hematoendothelial genes in a common cardiomyocyte-hematoendothelial mesoderm progenitor. However, only Etv2 itself and Tal1, not other ETV2-bound genes, were induced. Despite ETV2 genomic binding and Etv2 and Tal1 expression, cardiomyogenic fate potential was maintained. A second wave of ETV2-bound target genes was up-regulated during the transition from the common cardiomyocyte-hematoendothelial progenitor to the committed hematoendothelial population. A third wave of ETV-bound genes were subsequently expressed in the committed hematoendothelial population for sub-lineage differentiation. The shift from ETV2 binding to productive transcription, not ETV2 binding to target gene enhancers, drove hematoendothelial fate commitment. This work identifies mechanistic phases of ETV2-dependent gene expression that distinguish hematoendothelial specification, commitment, and differentiation.

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Project description:In this study, we directly reprogram adult human dermal fibroblasts (NHDF) into reprogrammed ECs (rECs) by overexpressing SOX17 in conjunction with ETV2. The rECs are capable of emulating in vitro and in vivo EC functions better than cells reprogrammed with ETV2 alone, such as improved reprogramming efficiency, enriched in more EC genes, and form large blood vessels carrying blood from the host, and most importantly, start to express eNOS in vivo. From these results, we present an improved method to reprogram adult fibroblasts into functional ECs and posit ideas for the future that could potentially further improve the reprogramming process.

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Comparison of Flk-1+/Etv2- vs Flk-1+/Etv2+ populations

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ETV2 cooperates with SCL for timely gene activation during hemogenic endothelium specification

Project description:ETV2 cooperates with SCL for timely gene activation during hemogenic endothelium specification

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