Alfonso A, Grundahl K, Duerr J S, Han H P, Rand J B
Program in Molecular and Cell Biology, Oklahoma Medical Research Foundation, Oklahoma City 73104.
Science. 1993 Jul 30;261(5121):617-9. doi: 10.1126/science.8342028.
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.
线虫秀丽隐杆线虫unc-17基因的突变会导致神经肌肉功能缺陷。该基因被克隆并对互补DNA进行了测序。基于与哺乳动物生物胺囊泡转运体的序列相似性以及在秀丽隐杆线虫胆碱能神经元突触小泡中的定位,unc-17可能编码乙酰胆碱囊泡转运体。消除所有unc-17基因功能的突变是致死性的,这表明乙酰胆碱转运体是必不可少的。对unc-17突变的分子分析将使基因(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子,后者可以鉴定编码与UNC-17相互作用蛋白质的基因。