Sheng, L., Leshchyns’ka, I., & Sytnyk, V.
School of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, 2052 New South Wales, Australia.
Changes in expression of the neural cell adhesion molecule 2 (NCAM2) have been proposed to contribute to neurodevelopmental disorders in humans. The role of NCAM2 in neuronal differentiation remains, however, poorly understood. Using genetically encoded Ca reporters, we show that clustering of NCAM2 at the cell surface of mouse cortical neurons induces submembrane [Ca2] spikes, which depend on the L-type voltage-dependent Ca2 channels (VDCCs) and require activation of the protein tyrosine kinase c-Src. We also demonstrate that clustering of NCAM2 induces L-type VDCC- and c-Src-dependent activation of CaMKII. NCAM2-dependent sub- membrane [Ca2] spikes colocalize with the bases of filopodia. NCAM2 activation increases the density of filopodia along neurites and neurite branching and out growth inanL-typeVDCC-, c-Src-, and CaMKII-dependent manner. Our results therefore indicate thatNCAM2 promotes the formation of filopodia and neurite branching by inducing Ca2 influx and CaMKII activation. Changes inNCAM2 expression in Down syndrome and autistic patients may therefore contribute to abnormal neurite branching observed in these disorders.
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The Journal of Neuroscience
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