Cassimeris L U, Wadsworth P, Salmon E D
J Cell Biol. 1986 Jun;102(6):2023-32. doi: 10.1083/jcb.102.6.2023.
Human monocytes, which contain few interphase microtubules (35.+/- 7.7), were used to study the dynamics of microtubule depolymerization. Steady-state microtubule assembly was abruptly blocked with either high concentrations of nocodazole (10 micrograms/ml) or exposure to cold temperature (3 degrees C). At various times after inhibition of assembly, cells were processed for anti-tubulin immunofluorescence microscopy. Stained cells were observed with an intensified video camera attached to the fluorescence microscope. A tracing of the entire length of each individual microtubule was made from the image on the television monitor by focusing up and down through the cell. The tracings were then digitized into a computer. All microtubules were seen to originate from the centrosome, with an average length in control cells of 7.1 +/- 2.7 microns (n = 957 microtubules). During depolymerization, the total microtubule polymer and the number of microtubules per cell decreased rapidly. In contrast, there was a slow decrease in the average length of the persisting microtubules. The half-time for both the loss of total microtubule polymer and microtubule number per cell was approximately 40 s for nocodazole-treated cells. The rate-limiting step in the depolymerization process was the rate of initiation of disassembly. Once initiated, depolymerization appeared catastrophic. Further kinetic analysis revealed two classes of microtubules: 70% of the microtubule population was very labile and initiated depolymerization at a rate approximately 23 times faster than a minor population of persistent microtubules. Cold treatment yielded qualitatively similar characteristics of depolymerization, but the initiation rates were slower. In both cases there was a significant asynchrony and heterogeneity in the initiation of depolymerization among the population of microtubules.
人单核细胞含有的间期微管较少(35±7.7),被用于研究微管解聚的动力学。用高浓度的诺考达唑(10微克/毫升)或低温(3℃)处理可突然阻断稳态微管组装。在组装抑制后的不同时间,对细胞进行抗微管蛋白免疫荧光显微镜检查。用连接到荧光显微镜的增强型摄像机观察染色后的细胞。通过在细胞中上下聚焦,从电视监视器上的图像追踪每个微管的全长。然后将追踪结果数字化输入计算机。所有微管均起源于中心体,对照细胞中微管的平均长度为7.1±2.7微米(n = 957根微管)。在解聚过程中,微管聚合物总量和每个细胞中的微管数量迅速减少。相比之下,持续存在的微管平均长度缓慢下降。对于用诺考达唑处理的细胞,微管聚合物总量和每个细胞中微管数量减少的半衰期约为40秒。解聚过程中的限速步骤是解聚起始速率。一旦起始,解聚似乎是灾难性的。进一步的动力学分析揭示了两类微管:70%的微管群体非常不稳定,起始解聚的速率比少数持续存在的微管快约23倍。冷处理产生了定性相似的解聚特征,但起始速率较慢。在这两种情况下,微管群体中解聚起始都存在明显的异步性和异质性。