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Fig. 6. A model for APC/ß-catenin interaction during neurite outgrowth. (A) In uninduced cells, active GSK3ß may phosphorylate APC and ß-catenin. Phosphorylated APC (APC^P) has a higher affinity for ß-catenin (Rubinfeld et al., 1996) and a lower affinity for microtubules (striped bar) (Zumbrunn et al., 2001). Phosphorylated ß-catenin (ß^P) is degraded. (B) In NGF-induced cells, NGF locally inactivates GSK3ß (Zhou et al., 2004), so GSK3ß may be inactive at the cell periphery and eventually the neurite tips, leading to local ß-catenin stabilization. Unphosphorylated APC has lower affinity for ß-catenin, so ß-catenin in the APC complex turns over rapidly. Unphosphorylated APC also binds and bundles microtubules, and this function at neurite tips may be regulated by its binding to ß-catenin. The ratio of free versus ß-catenin-bound APC could thereby determine microtubule bundling and neurite growth rate. The equilibrium would further shift toward neurite growth if ß-catenin levels are decreased, for example by being sequestered at adhesion sites, or if APC levels are increased, for example in response to NGF (Dobashi et al., 1996).

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