Balancing different types of actin polymerization at distinct sites: roles for Abelson kinase and Enabled.

Published

Journal Article

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 beta enhance abl phenotypes.

Full Text

Duke Authors

Cited Authors

  • Grevengoed, EE; Fox, DT; Gates, J; Peifer, M

Published Date

  • December 22, 2003

Published In

Volume / Issue

  • 163 / 6

Start / End Page

  • 1267 - 1279

PubMed ID

  • 14676307

Pubmed Central ID

  • 14676307

International Standard Serial Number (ISSN)

  • 0021-9525

Digital Object Identifier (DOI)

  • 10.1083/jcb.200307026

Language

  • eng

Conference Location

  • United States