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First published online May 16, 2007
doi: 10.1242/10.1242/dev.02849
1 Lineberger Comprehensive Cancer Center and Department of Biology, University
of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA.
2 Department of Biology, Bucknell University, Lewisburg, PA 17837, USA.
3 Department of Cell Biology and Program in Neuroscience, Harvard Medical
School, Boston, MA 02115, USA.
4 Massachusetts Institute of Technology, Department of Biology, Cambridge, MA
02139, USA.
* Author for correspondence (e-mail: peifer{at}unc.edu)
Accepted 12 March 2007
Studies in cultured cells and in vitro have identified many actin regulators and begun to define their mechanisms of action. Among these are Enabled (Ena)/VASP proteins, anti-Capping proteins that influence fibroblast migration, growth cone motility, and keratinocyte cell adhesion in vitro. However, partially redundant family members in mammals and maternal Ena contribution in Drosophila previously prevented assessment of the roles of Ena/VASP proteins in embryonic morphogenesis in flies or mammals. We used several approaches to remove maternal and zygotic Ena function, allowing us to address this question. We found that inactivating Ena does not disrupt cell adhesion or epithelial organization, suggesting its role in these processes is cell type-specific. However, Ena plays an important role in many morphogenetic events, including germband retraction, segmental groove retraction and head involution, whereas it is dispensable for other morphogenetic movements. We focused on dorsal closure, analyzing mechanisms by which Ena acts. Ena modulates filopodial number and length, thus influencing the speed of epithelial zippering and the ability of cells to match with correct neighbors. We also explored filopodial regulation in cultured Drosophila cells and embryos. These data provide new insights into developmental and mechanistic roles of this important actin regulator.
Key words: Ena/VASP, Epithelial morphogenesis, Cytoplasmic transport, Adhesion, Drosophila melanogaster
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