Driscoll M, Dean E, Reilly E, Bergholz E, Chalfie M
Department of Biological Sciences, Columbia University, New York 10027.
J Cell Biol. 1989 Dec;109(6 Pt 1):2993-3003. doi: 10.1083/jcb.109.6.2993.
Benzimidazole anti-microtubule drugs, such as benomyl, induce paralysis and slow the growth of the nematode Caenorhabditis elegans. We have identified 28 mutations in C. elegans that confer resistance to benzimidazoles. All resistant mutations map to a single locus, ben-1. Virtually all these mutations are genetically dominant. Molecular cloning and DNA sequence analysis established that ben-1 encodes a beta-tubulin. Some resistant mutants are completely deleted for the ben-1 gene. Since the deletion strains appear to be fully resistant to the drugs, the ben-1 product appears to be the only benzimidazole-sensitive beta-tubulin in C. elegans. Furthermore, since animals lacking ben-1 are viable and coordinated, the ben-1 beta-tubulin appears to be nonessential for growth and movement. The ben-1 function is likely to be redundant in the nematode genome.
苯并咪唑抗微管药物,如苯菌灵,可导致线虫秀丽隐杆线虫麻痹并减缓其生长。我们在秀丽隐杆线虫中鉴定出28个赋予对苯并咪唑抗性的突变。所有抗性突变都定位到一个单一基因座ben-1。实际上所有这些突变在遗传上都是显性的。分子克隆和DNA序列分析表明,ben-1编码一种β-微管蛋白。一些抗性突变体的ben-1基因完全缺失。由于缺失菌株似乎对药物完全抗性,ben-1产物似乎是秀丽隐杆线虫中唯一对苯并咪唑敏感的β-微管蛋白。此外,由于缺乏ben-1的动物是存活且协调的,ben-1β-微管蛋白似乎对生长和运动不是必需的。ben-1功能在线虫基因组中可能是冗余的。