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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]

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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.

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

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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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