Schulze K L, Broadie K, Perin M S, Bellen H J
Howard Hughes Medical Institute, Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030.
Cell. 1995 Jan 27;80(2):311-20. doi: 10.1016/0092-8674(95)90414-x.
Cloning and characterization of the Drosophila syntaxin-1A gene, syx-1A, reveal that it is present in several tissues but is predominantly expressed in the nervous system, where it is localized to axons and synapses. We have generated an allelic series of loss-of-function mutations that result in embryonic lethality with associated morphological and secretory defects dependent on the severity of the mutant allele. Electrophysiological recordings from partial loss-of-function mutants indicate absence of endogenous synaptic transmission at the neuromuscular junction and an 80% reduction of evoked transmission. Complete absence of syx-1A causes subtle morphological defects in the peripheral and central nervous systems, affects nonneural secretory events, and entirely abolishes neurotransmitter release. These data demonstrate that syntaxin plays a key role in nonneuronal secretion and is absolutely required for evoked neurotransmission.
果蝇 syntaxin-1A 基因（syx-1A）的克隆与特性分析表明，它存在于多个组织中，但主要在神经系统中表达，且定位于轴突和突触。我们已构建了一系列功能丧失型等位基因突变体，这些突变会导致胚胎致死，并伴有与突变等位基因严重程度相关的形态学和分泌缺陷。对部分功能丧失型突变体的电生理记录显示，神经肌肉接头处缺乏内源性突触传递，且诱发传递减少了 80%。syx-1A 的完全缺失会导致外周和中枢神经系统出现细微的形态学缺陷，影响非神经分泌事件，并完全消除神经递质释放。这些数据表明， syntaxin 在非神经元分泌中起关键作用，并且是诱发神经传递绝对必需的。
