THE CAENORHABDITIS-ELEGANS UNC-17 GENE - A PUTATIVE VESICULAR ACETYLCHOLINE TRANSPORTER
THE CAENORHABDITIS-ELEGANS UNC-17 GENE - A PUTATIVE VESICULAR ACETYLCHOLINE TRANSPORTER
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DOI：
10.1126/science.8342028
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发表时间：
1993-07-30
期刊：
影响因子：
56.9
通讯作者：
RAND, JB
中科院分区：
文献类型：
--
作者：
ALFONSO, A;GRUNDAHL, K;RAND, JB
线虫线虫的unc-17基因突变导致神经肌肉功能缺陷。克隆了该基因，并对互补DNA进行了测序。基于与哺乳动物生物胺囊泡转运蛋白的序列相似性和C.在线虫中，UNC-17可能编码乙酰胆碱的囊泡转运蛋白。消除所有unc-17基因功能的突变是致命的，这表明乙酰胆碱转运蛋白是必不可少的。对unc-17突变的分子分析将允许将基因（和蛋白质）的特定部分与观察到的功能缺陷相关联。这些突变体也将有助于分离基因外抑制因子，从而鉴定编码与β-17相互作用的蛋白质的基因。
Mutations in the unc-17 gene of the nematode Caenorhabditis elegans produce deficits in neuromuscular function. This gene was cloned and complementary DNAs were sequenced. On the basis of sequence similarity to mammalian vesicular transporters of biogenic amines and of localization to synaptic vesicles of cholinergic neurons in C. elegans, unc-17 likely encodes the vesicular transporter of acetylcholine. Mutations that eliminated all unc-17 gene function were lethal, suggesting that the acetylcholine transporter is essential. Molecular analysis of unc-17 mutations will allow the correlation of specific parts of the gene (and the protein) with observed functional defects. The mutants will also be useful for the isolation of extragenic suppressors, which could identify genes encoding proteins that interact with UNC-17.