Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
4343931 | Neuroscience Letters | 2013 | 5 Pages |
•Dendritic self-avoidance is critical for dendritic arborization neural circuits.•DSCAML1 promotes dendritic self-avoidance in newborn mouse cortical neurons.•Phosphorylation at Y1808 is essential in mediating the effects of DSCAML1.•The results shed light on the regulation mechanisms of dendrite arborization.
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 DSCAML1Y1808F 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.