A control structure of a nervous system synapse morphosis by a cell adhesion molecule.

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Nectins are Ca^<2+>-independent immunoglobulin-like cell-cell adhesion molecules and comprise a family of four members. At the mossy fiber terminals of hippocampus, nectin-1 and nectin-3 localize at the presynaptic and postsynaptic sides of synaptic junctions, respectively, and their trans-interaction plays a role in formation of synapses in cooperation with N-cadherin. Nectins are associated with the actin cytoskeleton through afadin, a nectin- and actin filament-binding protein. Inhibition of nectin-1-and nectin-3-based adhesion by in nectin-1 -/- mice resulted in the abnormal formation of synapses (Honda et al., 2006). Taken together, it is likely that nectins are involved in the formation of synapses in cooperation with N-cadherin. This role of nectins is consistent with the finding that mutations in the nectin-1 gene are responsible for cleft lip/palate-ectodermal dysplasia, which is characterized by mental retardation in addition to ectodermal dysplasia.For identification of a novel molecule that have cell-aggregation activity and is involved in synapse formation, we made a subtraction library for developmental hippocampus (P10-P5). This library was transfected into fibroblasts and the transfected cells were performed with cell-aggregation assay. We identified a voltage-gated K^+ channel as a cell adhesion molecule (Kimura et al., in preparation for submission). Furthermore, we also found that aquaproin 4, a water channel, has cell aggregation activity (Hiroaki et al. 2006).