The genetic correlation between synapse formation and memory

突触融合蛋白（syx）基因编码一种突触质膜蛋白，该蛋白与突触囊泡蛋白（如突触结合蛋白和小突触泡蛋白）一起调节突触囊泡释放。在syx突变体，自发囊泡释放是缺席的，突触后受体簇几乎没有形成。我们假设突触囊泡中含有聚集剂，囊泡的自发释放足以诱导突触后受体聚集。为了更准确地研究自发性囊泡胞吐的作用，我们分析了syx突变胚胎突触功能和形态的发育变化。在突触形成的早期阶段，我们发现在一个相当低的频率的方式表明母体Syx蛋白的贡献自发囊泡释放。与这一发现一致，很少观察到突触受体簇。然而，在syx突变体中，受体簇与突触面积的比率和簇的强度显著降低。此外，我们发现突触前缺陷syx突变体。突触分支数目减少，突触终扣肿胀，发育不良。这些结果表明，母体Syx蛋白有助于在突触形成的早期阶段残留的自发囊泡释放，并导致很少观察到的受体簇。syx调节突触前末梢的发育以及突触囊泡的释放。

The syntaxin (syx) gene encodes a synaptic plasma membrane protein that regulates synaptic vesicle release in association with synaptic vesicle protein such as synaptotagmin and synaptobrevin. In syx mutants, spontaneous vesicle release is absent, and postsynaptic receptor clusters are scarcely formed. We have hypothesized that synaptic vesicle contains clustering agent, and spontaneous vesicle release is sufficient to induce postsynaptic receptor clusters. In order to examine the role of spontaneous vesicle exocytosis more precisely, we analyze the developmental changes of synapse function and morphology in syx mutant embryos. At the early stage of synapse formation, we found spontaneous vesicle release in a quite low frequency manner suggesting contribution of maternal Syx protein. In consistent with this finding, synaptic receptor clusters were rarely observed. However, the ratio of the receptor cluster to synaptic area and intensity of clusters were significantly reduced in syx mutants. Furthermore, we found presynaptic defects in syx mutants. Number of synaptic branches were decreased, synaptic boutons swelled and less developed. These results suggest that maternal Syx protein contributes to residual spontaneous vesicle release at the early stage of synapse formation and Leads to rarely observed receptor clusters. syx regulates development of presynaptic terminals as well as synaptic vesicle release.