Stickel S K, Wang Y L
Department of Molecular and Cellular Biology, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206.
J Cell Biol. 1988 Sep;107(3):1231-9. doi: 10.1083/jcb.107.3.1231.
The synthetic peptide Gly-Arg-Gly-Asp-Ser (GRGDS) mimics the cellular binding site of many adhesive proteins in the extracellular matrix and causes rounding and detachment of spread cells. We have studied whether its binding affects the associations of two major components, alpha-actinin and vinculin, at the adhesion plaque. Living 3T3 cells were microinjected with fluorescently labeled alpha-actinin and/or vinculin and observed using video microscopy before and after the addition of 50 micrograms/ml GRGDS. As soon as 5 min after treatment, fluorescent alpha-actinin and vinculin became dissociated simultaneously from the sites of many focal contacts. The proteins either moved away as discrete structures or dispersed from adhesion plaques. As a result, the enrichment of alpha-actinin and vinculin at these focal contacts was no longer detected. The focal contacts then faded away slowly without showing detectable movement. These data suggest that the binding state of integrin has a transmembrane effect on the distribution of cytoskeletal components. The dissociation of alpha-actinin and vinculin from adhesion plaques may in turn weaken the contacts and result in rounding and detachment of cells.
合成肽甘氨酸 - 精氨酸 - 甘氨酸 - 天冬氨酸 - 丝氨酸(GRGDS)模拟细胞外基质中许多粘附蛋白的细胞结合位点,可导致铺展细胞变圆并脱离。我们研究了其结合是否会影响粘附斑处两个主要成分,即α - 辅肌动蛋白和纽蛋白的结合。将荧光标记的α - 辅肌动蛋白和/或纽蛋白显微注射到活的3T3细胞中,并在添加50微克/毫升GRGDS之前和之后使用视频显微镜进行观察。处理后5分钟,荧光α - 辅肌动蛋白和纽蛋白同时从许多粘着斑部位解离。这些蛋白质要么作为离散结构移开,要么从粘附斑处分散。结果,不再检测到α - 辅肌动蛋白和纽蛋白在这些粘着斑处的富集。然后粘着斑慢慢消失,未显示出可检测到的移动。这些数据表明整合素的结合状态对细胞骨架成分的分布具有跨膜效应。α - 辅肌动蛋白和纽蛋白从粘附斑的解离可能反过来削弱接触并导致细胞变圆和脱离。