Actin regulation in activity-dependent synaptic plasticity at the Drosophila neuromuscular junction

Synaptic plasticity is the process by which synaptic connections are continuously modified and is the molecular basis of learning and memory. These modifications require new protein synthesis and cytoskeletal rearrangements at or near the synapse. Syncrip, an mRNA-binding protein, is conserved from Drosophila to vertebrates and is found to regulate mRNAs encoding proteins required in synaptic plasticity. Many of these proteins have functions in actin-binding, actin cytoskeleton organization, or other actin-related processes, including Msp300, which was recently described in detail by the Davis lab. Here, we investigate two other targets of Syncrip, Basigin and Cofilin (Twinstar), among the most highly expressed of these genes in the Drosophila nervous system. By studying the activity-dependent synaptic plasticity, the change in neuronal connectivity as a result of activity, in the Drosophila neuromuscular junction, we showed that the loss of Cofilin in the presynapse leads to a decrease in activity-dependent synaptic plasticity, whereas the loss of Basigin in the postsynapse promotes plasticity. Deficiency of Basigin in the presynapse causes growth of larger boutons during development, while its effect during plasticity has yet to be determined. Furthermore, activity-induced expression of Basigin transcriptional level while the regulation of Cofilin takes place at posttranscriptional level. Basigin is present around some immature boutons. These data suggest that Basigin and Cofilin are involved in activity-dependent synaptic plasticity and have distinct roles in the pre- or postsynaptic compartments. Basigin could also play a part in the maturation of boutons. Our results add to the growing number of actin regulators that are downstream of Syncrip and have a role in neuronal plasticity.