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Rap2 and TNIK control Plexin-dependent tiled synaptic innervation in C. elegans
Ist Teil von
eLife, 2018-07, Vol.7
Ort / Verlag
England: eLife Sciences Publications Ltd
Erscheinungsjahr
2018
Link zum Volltext
Quelle
EZB Free E-Journals
Beschreibungen/Notizen
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 (
) and its effector, TNIK (
), act genetically downstream of Plexin (
) to restrict presynaptic assembly and to form tiled synaptic innervation in
. Both constitutively GTP- and GDP-forms of
mutants exhibit synaptic tiling defects as
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
mutants causes a severe synaptic tiling defect. Conversely, overexpression of
strongly inhibited synapse formation, suggesting that
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.