Etv5a regulates the proliferation of ventral mesoderm cells and the formation of hemato-vascular derivatives
- Authors
- Chen, S.Y., Shih, H.Y., Lin, S.J., Hsiao, C.D., Li, Z.C., and Cheng, Y.C.
- ID
- ZDB-PUB-131112-9
- Date
- 2013
- Source
- Journal of Cell Science 126(Pt 24): 5626-34 (Journal)
- Registered Authors
- Hsiao, Chung-Der, Lin, Sheng-Jia, Li, Zhi
- Keywords
- none
- MeSH Terms
-
- Animals
- Apoptosis
- Cell Differentiation
- Cell Proliferation*
- Embryo, Nonmammalian/cytology
- Embryo, Nonmammalian/metabolism
- Endothelial Cells/metabolism
- Endothelium, Vascular/cytology
- Gastrulation
- Gene Expression
- Gene Knockdown Techniques
- Mesoderm/cytology*
- Morpholinos/genetics
- Neovascularization, Physiologic
- Proto-Oncogene Proteins c-ets/physiology*
- Zebrafish/embryology*
- Zebrafish Proteins/physiology*
- PubMed
- 24101720 Full text @ J. Cell Sci.
Hematopoietic and vascular endothelial cells constitute the circulatory system and are both generated from the ventral mesoderm. However, the molecules and signaling pathways involved in ventral mesoderm formation and specification remain unclear. We found that zebrafish etv5a was expressed in the ventral mesoderm during gastrulation. Knockdown of Etv5a using morpholinos increased the proliferation of ventral mesoderm cells and caused defects in hematopoietic derivatives and in vascular formation. In contrast, the formation of other mesodermal derivatives, such as pronephros, somites and the gut wall, was not affected. Knockdown specificity was further confirmed by over-expression of an etv5a construct lacking its acidic domain. In conclusion, our data reveal that etv5a is essential for the inhibition of ventral mesoderm cell proliferation and for the formation of the hemato-vascular lineage.