Loss of β-catenin is not exactly disastrous. Mice with β-catenin deleted from hippocampal neurons after synapse formation showed normal levels of docked neurotransmitter vesicles, and broadly similar short-term responses to stimulation. But, in the mutants, nondocked vesicles were not as well localized at the site of action, so prolonged stimulation led to a faster drop-off in transmission. Similar results were seen in vitro after expression of a β-catenin lacking its PDZ-binding domain.
With β-catenin functioning as a scaffold, “it's not clear to me how much adhesion you need as opposed to signaling,” says Reichardt. “Cadherins do nucleate this diversity of signaling pathways. Whether you need contact [between axon and dendrite] because that nucleates something or contact because that puts you into position [for signaling] is not known.” ▪