Figure 9.

Ectopic SSR formation after strong GTX overexpression and proposed function of DLG and GTX during targeted membrane addition. A, B, Three-dimensional renderings of ectopic GTX-positive structures observed after overexpressing GTX with the strong C57 driver in wild type (A) and dlg^XI−2 mutant (B) backgrounds. Scale bar: A, B, 8 µm. C, Model of membrane trafficking to the postsynaptic region. In wild type, the presence of DLG at the postsynaptic membrane directs the fusion of GTX-positive vesicles to this site, forming the SSR. In dlg mutants, GTX targeting to the postsynaptic membrane is perturbed, resulting in reduced SSR expansion. When GTX is severely reduced in gtx mutants, despite the relatively normal synaptic DLG localization, fusion events are inhibited, and the SSR does not expand. When GTX is expressed at very high levels, inappropriate homotypic fusion occurs, leading to the formation of large vesicles and SSR-like structures in the cytoplasm and extrasynaptic muscle surface. D, Potential interactions between DLG and GTX during SSR formation. 1, GTX-positive vesicles are trafficked to the SSR, perhaps in a DLG dependent manner. 2, Through low-affinity interactions between DLG and GTX monomers, GTX-containing vesicles are concentrated at the SSR region. 3, Increased concentration of GTX-containing vesicles facilitates the formation of SNARE complexes, which are stabilized/protected by DLG. 4, The GTX SNARE complex formations allow the fusion of GTX vesicles with the SSR membrane, thus resulting in SSR expansion.