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Erg is a crucial regulator of endocardial-mesenchymal transformation during cardiac valve morphogenesis.


ABSTRACT: During murine embryogenesis, the Ets factor Erg is highly expressed in endothelial cells of the developing vasculature and in articular chondrocytes of developing bone. We identified seven isoforms for the mouse Erg gene. Four share a common translational start site encoded by exon 3 (Ex3) and are enriched in chondrocytes. The other three have a separate translational start site encoded by Ex4 and are enriched in endothelial cells. Homozygous Erg(?Ex3/?Ex3) knockout mice are viable, fertile and do not display any overt phenotype. By contrast, homozygous Erg(?Ex4/?Ex4) knockout mice are embryonic lethal, which is associated with a marked reduction in endocardial-mesenchymal transformation (EnMT) during cardiac valve morphogenesis. We show that Erg is required for the maintenance of the core EnMT regulatory factors that include Snail1 and Snail2 by binding to their promoter and intronic regions.

SUBMITTER: Vijayaraj P 

PROVIDER: S-EPMC3472597 | biostudies-literature | 2012 Nov

REPOSITORIES: biostudies-literature

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Erg is a crucial regulator of endocardial-mesenchymal transformation during cardiac valve morphogenesis.

Vijayaraj Preethi P   Le Bras Alexandra A   Mitchell Nora N   Kondo Maiko M   Juliao Saul S   Wasserman Meredith M   Beeler David D   Spokes Katherine K   Aird William C WC   Baldwin H Scott HS   Oettgen Peter P  

Development (Cambridge, England) 20120829 21


During murine embryogenesis, the Ets factor Erg is highly expressed in endothelial cells of the developing vasculature and in articular chondrocytes of developing bone. We identified seven isoforms for the mouse Erg gene. Four share a common translational start site encoded by exon 3 (Ex3) and are enriched in chondrocytes. The other three have a separate translational start site encoded by Ex4 and are enriched in endothelial cells. Homozygous Erg(ΔEx3/ΔEx3) knockout mice are viable, fertile and  ...[more]

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