Maduro M, Pilgrim D
Department of Biological Sciences, University of Alberta, Edmonton, Canada.
Genetics. 1995 Nov;141(3):977-88. doi: 10.1093/genetics/141.3.977.
A spontaneous mutation affecting locomotion of the nematode Caenorhabditis elegans has been mapped to a new gene, unc-119. Phenotypic characterization of the mutants suggests the defect does not lie in the musculature and that the animals also have defects in feeding behavior and chemosensation. unc-119 has been physically mapped relative to a previously identified chromosomal break in linkage group III, and DNA clones covering the region can rescue the mutant phenotype in transgenic animals. Three more alleles at the locus, with identical phenotypes, have been induced and characterized, all of which are putative null alleles. The predicted UNC-119 protein has no significant similarity to other known proteins. Expression of an unc-119/lacZ fusion in transgenic animals is seen in many neurons, suggesting that the unc-119 mutant phenotype is due to a defect in the nervous system.
一种影响秀丽隐杆线虫运动的自发突变已被定位到一个新基因unc-119。对这些突变体的表型特征分析表明,缺陷并不在于肌肉组织,而且这些动物在摄食行为和化学感受方面也存在缺陷。相对于之前在连锁群III中确定的染色体断裂点,unc-119已被进行了物理定位,覆盖该区域的DNA克隆可以挽救转基因动物中的突变体表型。在该基因座又诱导并鉴定出另外三个具有相同表型的等位基因,它们均为推定的无效等位基因。预测的UNC-119蛋白与其他已知蛋白没有显著相似性。在转基因动物中,许多神经元中都能看到unc-119/lacZ融合基因的表达,这表明unc-119突变体表型是由于神经系统缺陷所致。