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Molecular and Cellular Biology, October 2003, p. 7210-7221, Vol. 23, No. 20
0270-7306/03/$08.00+0     DOI: 10.1128/MCB.23.20.7210-7221.2003

Nckß Interacts with Tyrosine-Phosphorylated Disabled 1 and Redistributes in Reelin-Stimulated Neurons

Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1250

Received 23 January 2003/ Returned for modification 12 March 2003/ Accepted 10 July 2003

The tyrosine phosphorylation sites of the Disabled 1 (Dab1) docking protein are essential for the transmission of the Reelin signal, which regulates neuronal placement. Here we identify Nckß as a phosphorylation-dependent, Dab1-interacting protein. The SH2 domain of Nckß but not Nck binds Dab1 phosphorylated on the Reelin-regulated site, Y220, or on Y232. Nckß is coexpressed with Dab1 in the developing brain and in cultured neurons, where Reelin stimulation leads to the redistribution of Nckß from the cell soma into neuronal processes. We found that tyrosine-phosphorylated Dab1 in synergy with Nckß disrupts the actin cytoskeleton in transfected cells. In Drosophila melanogaster, exogenous expression of mouse Dab1 causes tyrosine phosphorylation site-dependent morphological changes in the compound eye. This phenotype is enhanced by overexpression of the Drosophila Nck protein Dock, suggesting a conserved interaction between the Disabled and Nck family members. We suggest a model in which Dab1 phosphorylation leads to the recruitment of Nckß to the membrane, where it acts to remodel the actin cytoskeleton.

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