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ZIRC
ZFIN ID: ZDB-PUB-090330-6
Discovery and characterization of novel vascular and hematopoietic genes downstream of etsrp in zebrafish
Gomez, G.A., Veldman, M.B., Zhao, Y., Burgess, S., and Lin, S.
Date: 2009
Source: PLoS One   4(3): e4994 (Journal)
Registered Authors: Burgess, Shawn, Gomez, Gustavo, Lin, Shuo, Veldman, Matt, Zhao, Yan
Keywords: Embryos, Zebrafish, Gene expression, Blood, Microarrays, Tails, Aorta, Endothelial cells
MeSH Terms:
  • Animals
  • Blood Vessels/growth & development
  • Embryo, Nonmammalian
  • Gene Expression Profiling
  • Gene Expression Regulation
  • Hematopoiesis/genetics*
  • Neovascularization, Physiologic/genetics*
  • Nerve Tissue Proteins/genetics*
  • Nerve Tissue Proteins/physiology
  • Proteoglycans/genetics*
  • Proteoglycans/physiology
  • Transcription Factors/genetics*
  • Transcription Factors/physiology
  • Zebrafish
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/physiology
PubMed: 19308258 Full text @ PLoS One
FIGURES
ABSTRACT
The transcription factor Etsrp is required for vasculogenesis and primitive myelopoiesis in zebrafish. When ectopically expressed, etsrp is sufficient to induce the expression of many vascular and myeloid genes in zebrafish. The mammalian homolog of etsrp, ER71/Etv2, is also essential for vascular and hematopoietic development. To identify genes downstream of etsrp, gain-of-function experiments were performed for etsrp in zebrafish embryos followed by transcription profile analysis by microarray. Subsequent in vivo expression studies resulted in the identification of fourteen genes with blood and/or vascular expression, six of these being completely novel. Regulation of these genes by etsrp was confirmed by ectopic induction in etsrp overexpressing embryos and decreased expression in etsrp deficient embryos. Additional functional analysis of two newly discovered genes, hapln1b and sh3gl3, demonstrates their importance in embryonic vascular development. The results described here identify a group of genes downstream of etsrp likely to be critical for vascular and/or myeloid development.
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