Breitfeld P P, McKinnon W C, Mostov K E
Department of Pediatrics (Hematology), University of Massachusetts Medical School, Worcester 01655.
J Cell Biol. 1990 Dec;111(6 Pt 1):2365-73. doi: 10.1083/jcb.111.6.2365.
A polarized cell, to maintain distinct basolateral and apical membrane domains, must tightly regulate vesicular traffic terminating at either membrane domain. In this study we have examined the extent to which microtubules regulate such traffic in polarized cells. Using the polymeric immunoglobulin receptor expressed in polarized MDCK cells, we have examined the effects of nocodazole, a microtubule-disrupting agent, on three pathways that deliver proteins to the apical surface and two pathways that deliver proteins to the basolateral surface. The biosynthetic and transcytotic pathways to the apical surface are dramatically altered by nocodazole in that a portion of the protein traffic on each of these two pathways is misdirected to the basolateral surface. The apical recycling pathway is slowed in the presence of nocodazole but targeting is not disrupted. In contrast, the biosynthetic and recycling pathways to the basolateral surface are less affected by nocodazole and therefore appear to be more resistant to microtubule disruption.
极化细胞为维持不同的基底外侧膜和顶端膜结构域，必须严格调控终止于任一膜结构域的囊泡运输。在本研究中，我们检测了微管在极化细胞中对这种运输的调控程度。利用极化的MDCK细胞中表达的聚合免疫球蛋白受体，我们检测了微管破坏剂诺考达唑对三条将蛋白质运输至顶端表面的途径以及两条将蛋白质运输至基底外侧表面的途径的影响。诺考达唑显著改变了至顶端表面的生物合成途径和转胞吞途径，因为这两条途径中每条途径上的一部分蛋白质运输被错误导向至基底外侧表面。在诺考达唑存在的情况下，顶端回收途径减慢，但靶向作用未被破坏。相比之下，至基底外侧表面的生物合成途径和回收途径受诺考达唑的影响较小，因此似乎对微管破坏更具抗性。
