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

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

Blog Article

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 Laser and party lighting 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 Beast Wars Plexin shapes proper synapse patterning in vivo.