Tyrosine phosphorylation is essential for DSCAML1 to promote dendrite arborization of mouse cortical neurons.

Dendritic self-avoidance is critical for appropriate dendrite arborization. We herein examined the role of Down syndrome cell adhesion molecule like-1 (DSCAML1) in regulating dendritic self-avoidance and that of tyrosine phosphorylation in mediating the effects of DSCAML1. Knocking down DSCAML1 in newborn mouse cortical neurons compromised dendritic self-avoidance as evidenced by dendritic fasciculation and increased dendritic self-crossing. Introduction of a DSCAML1(Y1808F) mutant into the DSCAML1-knocked down neurons failed to reverse the abnormal dendritic arborization. These results suggest that DSCAML1 promotes dendritic self-avoidance in cortical neurons, and that phosphorylation at Y1808 is essential in mediating the effects of DSCAML1.