GENETIC AND ELECTROPHYSIOLOGICAL STUDIES OF DROSOPHILA SYNTAXIN-1A DEMONSTRATE ITS ROLE IN NONNEURONAL SECRETION AND NEUROTRANSMISSION

GENETIC AND ELECTROPHYSIOLOGICAL STUDIES OF DROSOPHILA SYNTAXIN-1A DEMONSTRATE ITS ROLE IN NONNEURONAL SECRETION AND NEUROTRANSMISSION
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DOI:
10.1016/0092-8674(95)90414-x
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发表时间:
1995-01-27
期刊:
影响因子:
64.5
通讯作者:
BELLEN, HJ
BELLEN, HJ
中科院分区:
生物学1区
文献类型:
--
作者:
SCHULZE, KL;BROADIE, K;BELLEN, HJ

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对果蝇Syn Taxin-1A基因的克隆和鉴定表明,它存在于多种组织中,但主要在神经系统中表达,并定位于轴突和突触。我们已经产生了一系列功能丧失的突变,这些突变会导致胚胎死亡,并与相关的形态和分泌缺陷有关,这取决于突变等位基因的严重程度。部分功能丧失突变体的电生理记录表明,神经肌肉接头没有内源性突触传递,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微妙的形态缺陷,影响非神经分泌事件,并完全取消神经递质的释放。这些数据表明,突触素在非神经元分泌中起着关键作用,是诱发的神经传递所必需的。
Cloning and characterization of the Drosophila syn taxin-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.