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Published online 30 June 2003. doi:10.1083/jcb.200211025
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© The Rockefeller University Press, 0021-9525/2003/7/99 $5.00
The Journal of Cell Biology, Volume 162, Number 1, 99-111

Article

Dual regulation of neuronal morphogenesis by a {delta}-catenin–cortactin complex and Rho



Maria Cruz Martinez, Tomoyo Ochiishi, Michael Majewski and Kenneth S. Kosik

Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Harvard Institute of Medicine, Boston, MA 02115

Address correspondence to Kenneth S. Kosik, Dept. of Neurology, Brigham and Women's Hospital and Harvard Medical School, Harvard Institute of Medicine, 77 Ave. Louis Pasteur, Boston, MA 02115. Tel.: (617) 525-5230. Fax: (617) 525-5252. E-mail: kosik{at}cnd.bwh.harvard.edu

{delta}-Catenin is a neuronal protein that contains 10 Armadillo motifs and binds to the juxtamembrane segment of classical cadherins. We report that {delta}-catenin interacts with cortactin in a tyrosine phosphorylation–dependent manner. This interaction occurs within a region of the {delta}-catenin sequence that is also essential for the neurite elongation effects. Src family kinases can phosphorylate {delta}-catenin and bind to {delta}-catenin through its polyproline tract. Under conditions when tyrosine phosphorylation is reduced, {delta}-catenin binds to cortactin and cells extend unbranched primary processes. Conversely, increasing tyrosine phosphorylation disrupts the {delta}-catenin–cortactin complex. When RhoA is inhibited, {delta}-catenin enhances the effects of Rho inhibition on branching. We conclude that {delta}-catenin contributes to setting a balance between neurite elongation and branching in the elaboration of a complex dendritic tree.

Key Words: {delta}-catenin; cortactin; Rho; dendritic branching; tyrosine phosphorylation

* Abbreviations used in this paper: Arm, Armadillo; BDNF, brain-derived neurotrophic factor.


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