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First published online 3 January 2007
doi: 10.1242/dev.02748

Development 134, 567-578 (2007)
Published by The Company of Biologists 2007
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Abelson kinase (Abl) and RhoGEF2 regulate actin organization during cell constriction in Drosophila

Donald T. Fox1 and Mark Peifer1,2,*

1 Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-3280, USA.
2 Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-3280, USA.

* Author for correspondence (e-mail: peifer{at}unc.edu)

Accepted 20 November 2006

Morphogenesis involves the interplay of different cytoskeletal regulators. Investigating how they interact during a given morphogenetic event will help us understand animal development. Studies of ventral furrow formation, a morphogenetic event during Drosophila gastrulation, have identified a signaling pathway involving the G-protein Concertina (Cta) and the Rho activator RhoGEF2. Although these regulators act to promote stable myosin accumulation and apical cell constriction, loss-of-function phenotypes for each of these pathway members is not equivalent, suggesting the existence of additional ventral furrow regulators. Here, we report the identification of Abelson kinase (Abl) as a novel ventral furrow regulator. We find that Abl acts apically to suppress the accumulation of both Enabled (Ena) and actin in mesodermal cells during ventral furrow formation. Further, RhoGEF2 also regulates ordered actin localization during ventral furrow formation, whereas its activator, Cta, does not. Taken together, our data suggest that there are two crucial preconditions for apical constriction in the ventral furrow: myosin stabilization/activation, regulated by Cta and RhoGEF2; and the organization of apical actin, regulated by Abl and RhoGEF2. These observations identify an important morphogenetic role for Abl and suggest a conserved mechanism for this kinase during apical cell constriction.

Key words: Fog, G-alpha 12, G-alpha 13, Abl, Cta, Neural tube, S2 cell, Adherens junction, Drosophila




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