WAVE2 is required for directed cell migration and cardiovascular development

Daisuke Yamazaki, Shiro Suetsugu, Hiroaki Miki, Yuki Kataoka, Shin-Ichi Nishikawa, Takashi Fujiwara, Nobuaki Yoshida and Tadaomi Takenawa ()
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Daisuke Yamazaki: University of Tokyo
Shiro Suetsugu: University of Tokyo
Hiroaki Miki: University of Tokyo
Yuki Kataoka: University of Tokyo
Shin-Ichi Nishikawa: Kyoto University
Takashi Fujiwara: Ehime University School of Medicine
Nobuaki Yoshida: University of Tokyo
Tadaomi Takenawa: University of Tokyo

Nature, 2003, vol. 424, issue 6947, 452-456

Abstract: Abstract WAVE2, a protein related to Wiskott–Aldrich syndrome protein, is crucial for Rac-induced membrane ruffling, which is important in cell motility1,2,3,4. Cell movement is essential for morphogenesis, but it is unclear how cell movement is regulated or related to morphogenesis. Here we show the physiological functions of WAVE2 by disruption of the WAVE2 gene in mice. WAVE2 was expressed predominantly in vascular endothelial cells during embryogenesis. WAVE2-/- embryos showed haemorrhages and died at about embryonic day 10. Deficiency in WAVE2 had no significant effect on vasculogenesis, but it decreased sprouting and branching of endothelial cells from existing vessels during angiogenesis. In WAVE2-/- endothelial cells, cell polarity formed in response to vascular endothelial growth factor, but the formation of lamellipodia at leading edges and capillaries was severely impaired. These findings indicate that WAVE2-regulated actin reorganization might be required for proper cell movement and that a lack of functional WAVE2 impairs angiogenesis in vivo.

Date: 2003
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DOI: 10.1038/nature01770

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