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Ovol2/Movo , a homologue of Drosophila ovo , is required for angiogenesis, heart formation and placental development in mice
Author(s) -
Unezaki Sawako,
Horai Reiko,
Sudo Katsuko,
Iwakura Yoichiro,
Ito Seiji
Publication year - 2007
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2007.01084.x
Subject(s) - biology , angiogenesis , matrigel , microbiology and biotechnology , embryogenesis , embryonic stem cell , heart development , immunology , neovascularization , embryonic heart , andrology , anatomy , embryo , genetics , gene , medicine
The zinc‐finger transcription factor Ovol2 ( Movo , Movo2 ) is a mouse homologue of Drosophila ovo , which is essential for the survival and differentiation of female germ line cells. To elucidate OVOL2 function in mammals, we generated Ovol2 ‐deficient mice by gene targeting. The Ovol2 mutants died at embryonic days 9.5–10.5 (E9.5–E10.5), as a result of defects in extraembryonic and embryonic vascularization, and in heart formation. Although the Ovol2 expression was weak, severe defects were detected in extraembryonic and embryonic vascularization, and in heart formation at E8.5–E9.5. In Ovol2 −/− placentas, allantoic blood vessel expansion and development of the labyrinthine layer were impaired at E10.5. In an endothelial cell line, siRNAs for Ovol2 reduced the expression of Ovol2 and inhibited the capillary‐like network formation on Matrigel in vitro . These results demonstrate that Ovol2 may play a critical role in vascular angiogenesis during early embryogenesis.