Hasegawa T
School of Nursing, Kitasato University, Kanagawa, Japan.
J Cell Biol. 1993 Mar;120(6):1439-48. doi: 10.1083/jcb.120.6.1439.
I have produced a new monoclonal antibody, YF-169, against membrane ruffle specific 55-kD protein. YF-169 stained membrane ruffles of chick embryo fibroblasts so definitely that it enabled clear and reliable analyses of membrane ruffles. Fibroblasts organized two distinct types of membrane ruffles. One type of the ruffles were transiently formed in serum-starved cells (Type I) when stimulated by serum or platelet-derived growth factor. After spontaneous degradation of Type I ruffles, the other type of ruffles containing many microspikes were gradually organized at leading edges (Type II). The formation of Type I ruffles was not affected by either nocodazole, a microtubule-disrupting drug, or taxol, a microtubule-stabilizing reagent. However, Type II ruffles were entirely destroyed not only by nocodazole but also by taxol, suggesting that regulated organization of microtubule network is important to maintain Type II ruffles. H8, a protein kinase inhibitor prevented the spontaneous degradation of Type I ruffles and also reduced the destructive effect of nocodazole on Type II ruffles without affecting microtubule-disrupting activity. Protein kinases may be involved in the degradation processes of both types of ruffles. W7, a calmodulin antagonist, strongly inhibited Type I ruffle formation and completely destroyed Type II ruffles. W7 was also found to induce a remarkable change of 55-kD protein localization. After degradation of Type II ruffles, most of 55-kD protein was incorporated into newly formed unusual thick fibers. These results suggest that regulated organization of microtubule network is not necessary to form Type I ruffles but is important to maintain Type II ruffles, while calmodulin function is essential for both types of membrane ruffles.
我制备了一种新的单克隆抗体YF - 169,它针对膜皱襞特异性55-kD蛋白。YF - 169能清晰地标记鸡胚成纤维细胞的膜皱襞,从而能够对膜皱襞进行清晰可靠的分析。成纤维细胞形成两种不同类型的膜皱襞。一种皱襞是血清饥饿细胞(I型)在受到血清或血小板衍生生长因子刺激时短暂形成的。I型皱襞自发降解后,另一种含有许多微刺的皱襞在前沿逐渐形成(II型)。I型皱襞的形成不受微管破坏药物诺考达唑或微管稳定试剂紫杉醇的影响。然而,II型皱襞不仅会被诺考达唑完全破坏,也会被紫杉醇完全破坏,这表明微管网络的有序组织对于维持II型皱襞很重要。蛋白激酶抑制剂H8可阻止I型皱襞的自发降解,还能降低诺考达唑对II型皱襞的破坏作用,且不影响其微管破坏活性。蛋白激酶可能参与了两种类型皱襞的降解过程。钙调蛋白拮抗剂W7强烈抑制I型皱襞的形成,并完全破坏II型皱襞。还发现W7会引起55-kD蛋白定位的显著变化。II型皱襞降解后,大部分55-kD蛋白会整合到新形成的异常粗纤维中。这些结果表明,微管网络的有序组织对于形成I型皱襞不是必需的,但对于维持II型皱襞很重要,而钙调蛋白功能对于两种类型的膜皱襞都是必不可少的。