Mechanistically, Unc-51 inhibits the activity of the MAP kinase ERK to promote synaptic development. This decrease in synaptic density and abnormal active zone composition is associated with impaired evoked transmitter release. In addition to the presence of these aberrant synapses, there is also a decrease in the density of all synapses. In the absence of Unc-51, many glutamate receptor clusters are unapposed to Bruchpilot, and ultrastructural analysis demonstrates that fewer active zones contain dense body T-bars. Here we use a genetic analysis in Drosophila to demonstrate that the serine threonine kinase Unc-51 acts in the presynaptic motoneuron to regulate the localization of the active zone protein Bruchpilot opposite to glutamate receptors at each synapse. Many active zone proteins have been identified, but little is known of the mechanisms that ensure that each active zone receives the proper complement of proteins. Transmitter is released at active zones, which are composed of a large complex of proteins necessary for synaptic development and function. Efficient synaptic transmission requires the apposition of neurotransmitter release sites opposite clusters of postsynaptic neurotransmitter receptors.
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