Aszalos A, Yang G C, Gottesman M M
J Cell Biol. 1985 May;100(5):1357-62. doi: 10.1083/jcb.100.5.1357.
Depolymerization of microtubules resulted in an increase in the motional freedom of molecular probes in the plasma membranes of Chinese hamster ovary cells expressed by the order parameter, S, measured with two different lipid-soluble spin label probes, 5-doxyl stearic acid and 16-doxyl methylstearate. Treatment with a variety of microtubule-depolymerizing agents, including Colcemid, colchicine, vinblastine, podophyllotoxin, and griseofulvin, all had similar effects on motional freedom of the probes whereas beta-lumicolchicine was inactive. Several independent lines of evidence suggest that these changes in motional freedom of the probes were not the direct result of the interaction of these relatively hydrophobic drugs with the plasma membrane: the effects of the drugs were not immediate; the dose response of the Colcemid effect was the same as the dose response for depolymerization of microtubules; taxol, which stabilizes microtubules but does not affect motional freedom in the membranes, blocked the effect of Colcemid on motional freedom; a mutant cell line which is resistant to colchicine because of reduced uptake of the drug showed no effects of colchicine on probe motional freedom; and a Colcemid-resistant mutant cell line with an altered beta-tubulin showed no effect of Colcemid on motional freedom in the membrane. These results support the hypothesis that microtubules might affect, directly or indirectly, plasma membrane functions.
微管解聚导致中国仓鼠卵巢细胞膜中分子探针运动自由度增加，这一增加通过序参数S来表示，该参数是用两种不同的脂溶性自旋标记探针，即5-多昔硬脂酸和16-多昔甲基硬脂酸来测量的。用多种微管解聚剂处理，包括秋水仙酰胺、秋水仙碱、长春碱、鬼臼毒素和灰黄霉素，所有这些试剂对探针的运动自由度都有类似的影响，而β-光秋水仙碱则无活性。几条独立的证据表明，探针运动自由度的这些变化并非这些相对疏水的药物与质膜相互作用的直接结果：药物的作用并非立即显现；秋水仙酰胺作用的剂量反应与微管解聚的剂量反应相同；紫杉醇可稳定微管但不影响膜中的运动自由度，它能阻断秋水仙酰胺对运动自由度的影响；一种因药物摄取减少而对秋水仙碱耐药的突变细胞系，秋水仙碱对其探针运动自由度无影响；还有一种具有改变的β-微管蛋白的秋水仙酰胺耐药突变细胞系，秋水仙酰胺对其膜中的运动自由度也无影响。这些结果支持了微管可能直接或间接影响质膜功能这一假说。
