Oakley B R, Morris N R
Cell. 1981 Jun;24(3):837-45. doi: 10.1016/0092-8674(81)90109-4.
We have isolated a heat-sensitive beta-tubulin mutation, benA33, that blocks nuclear division and nuclear movement at restrictive temperature. This blockage demonstrates that the beta tubulin encoded by the benA gene is essential to both processes. The blockage of both processes is suppressed by the alpha-tubulin mutation, tubA1; thus the alpha tubulin encoded by the tubA gene must also be involved in both processes. When benA33 is shifted from a permissive to restrictive temperature, nuclei are blocked in mitosis. Light microscopy of blocked nuclei reveals that benA33 inhibits movement of chromosomes to the poles, and electron microscopy of blocked nuclei shows that they contain apparently normal spindles. Thus benA33 does not block microtubule assembly but, directly or indirectly, blocks microtubule disassembly. BenA33 also confers resistance to several antimicrotubule agents and the heat sensitivity conferred by benA33 is suppressed by each of these agents. We suggest that the simplest explanation for these effects is that benA33 causes a temperature-dependent hyperstabilization of microtubules that blocks chromosomal movement by blocking microtubule disassembly.
我们分离出了一种温度敏感型β-微管蛋白突变体benA33,在限制温度下它会阻断核分裂和核移动。这种阻断表明benA基因编码的β-微管蛋白对这两个过程都是必不可少的。α-微管蛋白突变体tubA1可抑制这两个过程的阻断;因此tubA基因编码的α-微管蛋白也必定参与这两个过程。当benA33从允许温度转变为限制温度时,细胞核在有丝分裂过程中被阻断。对被阻断细胞核的光学显微镜观察显示,benA33抑制染色体向两极移动,对被阻断细胞核的电子显微镜观察表明,它们含有明显正常的纺锤体。因此,benA33并不阻断微管组装,而是直接或间接地阻断微管解聚。BenA33还赋予对几种抗微管药物的抗性,并且这些药物中的每一种都能抑制benA33所赋予的温度敏感性。我们认为,对这些效应最简单的解释是,benA33导致微管的温度依赖性超稳定,通过阻断微管解聚来阻断染色体移动。