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Neuropil Pattern Formation and Regulation of Cell Adhesion Molecules in Drosophila Optic Lobe Development Depend on Synaptobrevin

机译:果蝇视神经叶发育过程中Neuropil模式的形成和细胞粘附分子的调节取决于突触臂蛋白。

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摘要

To investigate a possible involvement of synaptic machinery inDrosophila visual system development, we studied the effects of a loss of function of neuronal synaptobrevin, a protein required for synaptic vesicle release. Expression of tetanus toxin light chain (which cleaves neuronal synaptobrevin) and genetic mosaics were used to analyze neuropil pattern formation and levels of selected neural adhesion molecules in the optic lobe. We show that targeted toxin expression in the developing optic lobe results in disturbances of the columnar organization of visual neuropils and of photoreceptor terminal morphology. IrreC-rst immunoreactivity in neuropils is increased after widespread expression of toxin. In photoreceptors, targeted toxin expression results in increased Fasciclin II and chaoptin but not IrreC-rst immunoreactivity. Axonal pathfinding and programmed cell death are not affected. In genetic mosaics, patches of photoreceptors that lack neuronal synaptobrevin exhibit the same phenotypes observed after photoreceptor-specific toxin expression. Our results demonstrate the requirement of neuronal synaptobrevin for regulation of cell adhesion molecules and development of the fine structure of the optic lobe. A possible causal link to fine-tuning processes that may include synaptic plasticity in the development of the Drosophila CNS is discussed.
机译:为了研究果蝇视觉系统发育中突触机制的可能参与,我们研究了神经元突触短纤维蛋白(突触小泡释放所需的蛋白质)功能丧失的影响。破伤风毒素轻链(可切割神经元突触连接蛋白)的表达和遗传镶嵌结构可用于分析视神经叶中神经纤维的形成和所选神经粘附分子的水平。我们表明在发展中的视神经叶中有针对性的毒素表达导致视觉神经柱和光感受器终端形态的柱状组织的紊乱。毒素广泛表达后,神经纤维中的IrreC-rst免疫反应性增加。在光感受器中,靶向毒素的表达导致Fasciclin II和Chaoptin的增加,但不会导致IrreC-rst免疫反应。轴突寻路和程序性细胞死亡不受影响。在遗传马赛克中,缺乏神经元突触短纤维蛋白的感光细胞斑块表现出在感光细胞特异性毒素表达后观察到的相同表型。我们的研究结果表明神经元突触短纤维蛋白调节细胞粘附分子和发展视神经叶的精细结构的要求。讨论了与果蝇中枢神经系统发育过程中可能包括突触可塑性的微调过程的可能因果关系。

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