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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE92537 | GEO | 2017/12/12

SECONDARY ACCESSION(S): PRJNA357990

REPOSITORIES: GEO

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

Project description:By comparing SCL binding in day 4 Etv2KOiSCL and Etv2KOiETV2 mesodermal cells to WT, we showed delayed gene activation or repression could not be simly explained by loss of SCL binding in Etv2KOiSCL mesodermal cells

2017-12-12 | GSE92536 | GEO

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

2017-12-12 | GSE92535 | GEO

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

Project description: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.

2017-12-12 | GSE92534 | GEO

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

| PRJNA357990 | ENA

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+Pdgfr?+ 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 Scl(fl/fl)Rosa26Cre-ER(T2) 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.

| S-EPMC3624753 | biostudies-literature

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers

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

2015-01-01 | E-GEOD-47085 | biostudies-arrayexpress

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.

| S-EPMC9060440 | biostudies-literature

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers

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

2015-01-01 | GSE47085 | GEO

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

Project description:The transcriptional factor GATA2 is required for blood and hematopoietic stem cell formation during the hemogenic endothelium (HE) stage of development in the embryo. However, it is unclear if GATA2 controls HE lineage specification or if it solely regulates endothelial-to-hematopoietic transition (EHT). To address this problem, we innovated a unique system, which involved generating GATA2 knockout human embryonic stem cell (hESC) lines with conditional GATA2 expression (iG2-/- hESCs). We demonstrated that GATA2 activity is not required for VE-cadherin+CD43-CD73+ non-HE or VE-cadherin+CD43-CD73- HE generation and subsequent HE diversification into DLL4+ arterial and DLL4- non-arterial lineages. However, GATA2 is primarily needed for HE to undergo EHT. Forced expression of GATA2 in non-HE failed to induce blood formation. The lack of GATA2 requirement for generation of HE and non-HE indicates the critical role of GATA2-independent pathways in specification of these two distinct endothelial lineages.

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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.

2012-08-03 | GSE27445 | GEO

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