Synaptogenesis involves the transformation of a growth cone into synaptic boutons specialized for transmitter release. In Drosophila embryos lacking the α 2β-3 subunit of presynaptic, voltage-dependent Ca 2+ channels, we found that motor neuron terminals failed to develop synaptic boutons and cytoskeletal abnormalities arose, including the loss of ankyrin2. Nevertheless, functional presynaptic specializations were present and apposed to clusters of postsynaptic glutamate receptors. The α 2β-3 protein has been thought to function strictly as an auxiliary subunit of the Ca 2+ channel, but the phenotype of α 2β-3 (also known as stj) mutations cannot be explained by a channel defect; embryos lacking the pore-forming α1 subunit cacophony formed boutons. The synaptogenic function of α 2β-3 required only the α2 peptide, whose expression sufficed to rescue bouton formation. Our results indicate that α 2β proteins have functions that are independent of their roles in the biophysics and localization of Ca 2+ channels and that synaptic architecture depends on these functions.
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