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Transcriptional inhibition of etv2 expression is essential for embryonic cardiac development.


ABSTRACT: E-twenty six variant 2 (Etv2) transcription factor participates in cardiac, vascular-endothelial and blood cell lineage specification decisions during embryonic development. Previous studies have identified genomic elements in the etv2 locus responsible for vascular endothelial cell specification. Using transgenic analysis in zebrafish, we report here an etv2 proximal promoter fragment that prevents transgene misexpression in myocardial progenitor cells. This inhibition of etv2 expression in the cardiac progenitor population is partly mediated by Scl and Nkx2.5, likely through direct binding to the etv2 promoter, and cis-regulatory elements located in the first and second introns. The results identify an etv2 cis-regulatory mechanism controlling cardiovascular fate choice implying that etv2 participates in a transcriptional network mediating developmental plasticity of endothelial progenitor cells during embryonic development.

SUBMITTER: Schupp MO 

PROVIDER: S-EPMC4137469 | biostudies-literature | 2014 Sep

REPOSITORIES: biostudies-literature

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Transcriptional inhibition of etv2 expression is essential for embryonic cardiac development.

Schupp Marcus-Oliver MO   Waas Matthew M   Chun Chang-Zoon CZ   Ramchandran Ramani R  

Developmental biology 20140628 1


E-twenty six variant 2 (Etv2) transcription factor participates in cardiac, vascular-endothelial and blood cell lineage specification decisions during embryonic development. Previous studies have identified genomic elements in the etv2 locus responsible for vascular endothelial cell specification. Using transgenic analysis in zebrafish, we report here an etv2 proximal promoter fragment that prevents transgene misexpression in myocardial progenitor cells. This inhibition of etv2 expression in the  ...[more]

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