Synaptic cell adhesion molecules (SCAMs) are mostly membrane-anchored molecules with extracellular domains that extend into the synaptic cleft. Prototypical SCAMs interact with homologous or heterologous molecules on the surface of adjacent cells, ensuring precise apposition of pre- and postsynaptic elements. More recent definitions of SCAMs often include molecules involved in axon pathfinding, cell recognition and synaptic differentiation events, making SCAMs functionally and molecularly a very diverse group.

In contrast to the substantial effect that some knockout mouse models of molecules involved in synaptic vesicle release yield, no SCAM mutant has been reported thus far that would show a prominently altered structure of the majority of synapses, or even lack synapses altogether. This surprising resilience of the synaptic structure could be explained by high redundancy between different SCAMs, by the assumption that the crucial molecular players in synapse structure have yet to be discovered, or by a grand variability in the mechanisms of synapse formation that underlies the diversity of synapses.

In this project, we try to identify yet unknown players at the synapse by differential display and proteomics approaches, comparing different developmental stages, different types of synapses, and wild type vs. mutant animals that lack MeCP2, a transcriptional repressor responsible for Rett syndrome.