Development and plasticity of synapses are brought about by a complex interplay between various signaling pathways. Typically, either changing the number of synapses or strengthening an existing synapse can lead to changes during synaptic plasticity. Altering the machinery that governs the exocytosis of synaptic vesicles, which primarily fuse at specialized structures known as active zones on the presynaptic terminal, brings about these changes. Although signaling pathways that regulate the synaptic plasticity from the postsynaptic compartments are well defined, the pathways that control these changes presynaptically are poorly described. In a genetic screen for synapse development in Drosophila, we found that mutations in CK2α lead to an increase in the levels of Bruchpilot (BRP), a scaffolding protein associated with the active zones. Using a combination of genetic and biochemical approaches, we found that the increase in BRP in CK2α mutants is largely due to an increase in the transcription of BRP. Interestingly, the transcripts of other active zone proteins that are important for function of active zones were also increased, while the transcripts from some other synaptic proteins were unchanged. Thus, our data suggest that CK2α might be important in regulating synaptic plasticity by modulating the transcription of BRP. Hence, we propose that CK2α is a novel regulator of the active zone protein, BRP, in Drosophila.
Keywords: Active zone; Bruchpilot; Drosophila; Neuromuscular junction; Synapse; Synapse development.
© 2013 Published by Elsevier Inc.