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During development, neurons form synapses with their fate-determined targets. While we begin to elucidate the mechanisms by which extracellular ligand-receptor interactions enhance synapse specificity by inhibiting synaptogenesis, our knowledge about their intracellular mechanisms remains limited. Here we show that Rap2 GTPase ( rap-2 ) and its effector, TNIK ( mig-15 ), act genetically downstream of Plexin ( plx-1 ) to restrict presynaptic assembly and to form tiled synaptic innervation in  C. elegans . Both constitutively GTP- and GDP-forms of  rap-2  mutants exhibit synaptic tiling defects as  plx-1  mutants, suggesting that cycling of the RAP-2 nucleotide state is critical for synapse inhibition. Consistently, PLX-1 suppresses local RAP-2 activity. Excessive ectopic synapse formation in  mig-15  mutants causes a severe synaptic tiling defect. Conversely, overexpression of  mig-15  strongly inhibited synapse formation, suggesting that  mig-15  is a negative regulator of synapse formation. These results reveal that subcellular regulation of small GTPase activity by Plexin shapes proper synapse patterning in vivo.

Rap2 and TNIK control Plexin-dependent tiled synaptic innervation in C. elegans