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

Preethi Vijayaraj | Zendy; Alexandra Le Bras | Zendy; Nora Mitchell | Zendy; Maiko Kondo | Zendy; Saul F. Juliao | Zendy; Meredith Wasserman | Zendy; David Beeler | Zendy; Katherine Spokes | Zendy; William C. Aird | Zendy; H. Scott Baldwin | Zendy; Peter Oettgen | Zendy

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

Author(s) -

Preethi Vijayaraj,

Alexandra Le Bras,

Nora Mitchell,

Maiko Kondo,

Saul F. Juliao,

Meredith Wasserman,

David Beeler,

Katherine Spokes,

William C. Aird,

H. Scott Baldwin,

Peter Oettgen

Publication year - 2012

Publication title -

development

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.754

H-Index - 325

eISSN - 1477-9129

pISSN - 0950-1991

DOI - 10.1242/dev.081596

Subject(s) - biology , erg , mesenchymal stem cell , phenotype , regulator , microbiology and biotechnology , knockout mouse , conditional gene knockout , heart development , embryonic stem cell , gene isoform , morphogenesis , gene , transcription factor , genetics , neuroscience , retina

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 do not display any overt phenotype. By contrast, homozygous Erg(ΔEx4/ΔEx4) 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.

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