Vasquez R J, Howell B, Yvon A M, Wadsworth P, Cassimeris L
Department of Biological Sciences, Lehigh University, Bethlehem, Pennsylvania 18015, USA.
Mol Biol Cell. 1997 Jun;8(6):973-85. doi: 10.1091/mbc.8.6.973.
Previous studies demonstrated that nanomolar concentrations of nocodazole can block cells in mitosis without net microtubule disassembly and resulted in the hypothesis that this block was due to a nocodazole-induced stabilization of microtubules. We tested this hypothesis by examining the effects of nanomolar concentrations of nocodazole on microtubule dynamic instability in interphase cells and in vitro with purified brain tubulin. Newt lung epithelial cell microtubules were visualized by video-enhanced differential interference contrast microscopy and cells were perfused with solutions of nocodazole ranging in concentration from 4 to 400 nM. Microtubules showed a loss of the two-state behavior typical of dynamic instability as evidenced by the addition of a third state where they exhibited little net change in length (a paused state). Nocodazole perfusion also resulted in slower elongation and shortening velocities, increased catastrophe, and an overall decrease in microtubule turnover. Experiments performed on BSC-1 cells that were microinjected with rhodamine-labeled tubulin, incubated in nocodazole for 1 h, and visualized by using low-light-level fluorescence microscopy showed similar results except that nocodazole-treated BSC-1 cells showed a decrease in catastrophe. To gain insight into possible mechanisms responsible for changes in dynamic instability, we examined the effects of 4 nM to 12 microM nocodazole on the assembly of purified tubulin from axoneme seeds. At both microtubule plus and minus ends, perfusion with nocodazole resulted in a dose-dependent decrease in elongation and shortening velocities, increase in pause duration and catastrophe frequency, and decrease in rescue frequency. These effects, which result in an overall decrease in microtubule turnover after nocodazole treatment, suggest that the mitotic block observed is due to a reduction in microtubule dynamic turnover. In addition, the in vitro results are similar to the effects of increasing concentrations of GDP-tubulin (TuD) subunits on microtubule assembly. Given that nocodazole increases tubulin GTPase activity, we propose that nocodazole acts by generating TuD subunits that then alter dynamic instability.
先前的研究表明,纳摩尔浓度的诺考达唑可使细胞阻滞于有丝分裂期,而不会导致微管的净解聚,从而产生了这样一种假说,即这种阻滞是由于诺考达唑诱导的微管稳定所致。我们通过检测纳摩尔浓度的诺考达唑对间期细胞微管动态不稳定性的影响以及在体外对纯化的脑微管蛋白的影响,来验证这一假说。通过视频增强微分干涉相差显微镜观察蝾螈肺上皮细胞微管,并向细胞灌注浓度范围为4至400 nM的诺考达唑溶液。微管表现出动态不稳定性典型的双态行为丧失,这表现为出现了第三种状态,即它们的长度几乎没有净变化(一种暂停状态)。诺考达唑灌注还导致伸长和缩短速度减慢、灾变增加以及微管周转率总体下降。对注射了罗丹明标记微管蛋白的BSC-1细胞进行实验,在诺考达唑中孵育1小时,并用微光水平荧光显微镜观察,结果相似,只是经诺考达唑处理的BSC-1细胞灾变减少。为了深入了解导致动态不稳定性变化的可能机制,我们检测了4 nM至12 μM诺考达唑对来自轴丝种子的纯化微管蛋白组装的影响。在微管的正端和负端,用诺考达唑灌注均导致伸长和缩短速度呈剂量依赖性下降、暂停持续时间和灾变频率增加以及挽救频率下降。这些效应导致诺考达唑处理后微管周转率总体下降,表明观察到的有丝分裂阻滞是由于微管动态周转率降低所致。此外,体外实验结果与增加GDP-微管蛋白(TuD)亚基浓度对微管组装的影响相似。鉴于诺考达唑会增加微管蛋白GTP酶活性,我们提出诺考达唑的作用方式是产生TuD亚基,进而改变动态不稳定性。