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This review addresses our current understanding of the regulatory mechanisms for classical cadherin expression during development of the vertebrate nervous system. The complexity of the spatial and temporal expression patterns is linked to morphogenic and functional roles in the developing nervous system. While the regulatory networks controlling cadherin expression are not well understood, it is likely that the multiple signaling pathways active in the development of particular domains also regulate the specific cadherins expressed at that time and location. With the growing understanding of the broader roles of cadherins in cell-cell adhesion and non-adhesion processes, it is important to understand both the upstream regulation of cadherin expression and the downstream effects of specific cadherins within their cellular context.

The catenin ARVCF is a member of the p120 ctn subfamily of Armadillo proteins. A number of catenins directly bind cadherin cytoplasmic tails, contributing to the modulation of cell-cell adhesion and motility processes. Some catenins, such as ␤-catenin (and likely p120 ctn ), have additional roles within signaling pathways regulating gene transcription. We have isolated the Xenopus homolog of human ARVCF. Utilizing the cadherin membrane proximal region known to bind p120 ctn and ␦-catenin, coimmunoprecipitation experiments demonstrate that Xarvcf, likewise, binds cadherin in this region and that corresponding point mutations within conserved residues abrogate the Xarvcfcadherin association. Western blot analysis of Xarvcf protein across a series of developmental stages reveals changes in protein mobility, likely due to changes in phosphorylation. Xarvcf is a maternally provided transcript and expressed in the embryo throughout all stages of development. Interestingly, Xarvcf mRNA is differentially spliced to produce several isoforms, one of which is developmentally regulated. In common with the putative post-translational modifications of the Xarvcf protein, the presence of alternative splice isoforms suggests that Xarvcf possesses the capacity to effect developmental functions in a regulatable manner.