Published online 15 December 2003. doi:10.1083/jcb.200307026
© The Rockefeller University Press,
0021-9525/2003/12/1267 $8.00
The Journal of Cell Biology, Volume 163, Number 6, 1267-1279
Balancing different types of actin polymerization at distinct sites
:
roles for Abelson kinase and Enabled
Elizabeth E. Grevengoed1,
Donald T. Fox2,
Julie Gates3 and
Mark Peifer1,2,3
1 Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599
2 Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599
3 Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599
Address correspondence to Mark Peifer, Dept. of Biology, Coker Hall, CB #3280, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-3280. Tel.: (919) 962-2271. Fax: (919) 962-1625. email: peifer{at}unc.edu
The proto-oncogenic kinase Abelson (Abl) regulates actin in response to cell signaling. Drosophila Abl is required in the nervous system, and also in epithelial cells, where it regulates adherens junction stability and actin organization. Abl acts at least in part via the actin regulator Enabled (Ena), but the mechanism by which Abl regulates Ena is unknown. We describe a novel role for Abl in early Drosophila development, where it regulates the site and type of actin structures produced. In Abl's absence, excess actin is polymerized in apical microvilli, whereas too little actin is assembled into pseudocleavage and cellularization furrows. These effects involve Ena misregulation. In abl mutants, Ena accumulates ectopically at the apical cortex where excess actin is observed, suggesting that Abl regulates Ena's subcellular localization. We also examined other actin regulators. Loss of Abl leads to changes in the localization of the Arp2/3 complex and the formin Diaphanous, and mutations in diaphanous or capping protein ß enhance abl phenotypes.
Key Words: adherens junctions; Arp 2/3; formins; capping protein; cellularization
D. Fox and J. Gates contributed equally to this paper.
The online version of this article includes supplemental material.
Abbreviations used in this paper: Abl, Abelson; ablM, abl maternal mutant;
-cat,
-catenin; AJ, adherens junction; Arg, Abl-related gene; Arm, Armadillo; cpb, capping protein ß; CNS, central nervous system; Dia, Diaphanous; Ena, Enabled; VASP, vasodilator-stimulated phosphoprotein.

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