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

ABSTRACT: By performing ATAC sequencing in WT, Etv2KoiSCL and Etv2KOiETV2 ES cell derived day 4.75 endothelial cells, we report here ETV2 increases chromatin accessiblity at its binding sites.

ORGANISM(S): Mus musculus

PROVIDER: GSE92534 | GEO | 2017/12/12

SECONDARY ACCESSION(S): PRJNA358000

REPOSITORIES: GEO

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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 cooperates with SCL for timely gene activation during hemogenic endothelium specification

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

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

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Scl represses cardiomyogenesis in prospective hemogenic endothelium and endocardium.

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Hemogenic and aortic endothelium arise from a common hemogenic angioblast precursor and are specified by the Etv2 dosage.

Project description:SignificanceHematopoietic stem cells (HSCs) are generated from specialized endothelial cells, called hemogenic endothelial cells (HECs). It has been debated whether HECs and non-HSC-forming conventional endothelial cells (cECs) arise from a common precursor or represent distinct lineages. Moreover, the molecular basis underlying their distinct fate determination is poorly understood. We use photoconvertible labeling, time-lapse imaging, and single-cell RNA-sequencing analysis to trace the lineage of HECs. We discovered that HECs and cECs arise from a common hemogenic angioblast precursor, and their distinct fate is determined by high or low dosage of Etv2, respectively. Our results illuminate the lineage origin and a mechanism on the fate determination of HECs, which may enhance the understanding on the ontogeny of HECs in vertebrates.

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

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GATA2 Is Dispensable for Specification of Hemogenic Endothelium but Promotes Endothelial-to-Hematopoietic Transition.

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Scl Represses Cardiomyogenesis in Prospective Hemogenic Endothelium and Endocardium

Project description:Endothelium in embryonic hematopoietic tissues generates hematopoietic stem/progenitor cells; however, it is unknown how its unique potential is specified. We show that transcription factor Scl/Tal1 is essential for both establishing the hematopoietic transcriptional program in hemogenic endothelium and preventing its misspecification to a cardiomyogenic fate. Scl-/- embryos activated a cardiac transcriptional program in yolk sac endothelium, leading to the emergence of CD31+Pdgfrα+ cardiogenic precursors that generated spontaneously beating cardiomyocytes. Ectopic cardiogenesis was also observed in Scl-/- hearts, where the disorganized endocardium precociously differentiated into cardiomyocytes. Induction of mosaic deletion of Scl in Sclfl/flRosa26Cre-ERT2 embryos revealed a cell-intrinsic, temporal requirement for Scl to prevent cardiomyogenesis from endothelium. Scl-/- endothelium also upregulated the expression of Wnt antagonists, which promoted rapid cardiomyocyte differentiation of ectopic cardiogenic cells. These results reveal unexpected plasticity in embryonic endothelium such that loss of a single master regulator can induce ectopic cardiomyogenesis from endothelial cells.

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