Kraft T, Messerli M, Rothen-Rutishauser B, Perriard J C, Wallimann T, Brenner B
Department of Clinical Physiology, Medical School of Hannover, Germany.
Biophys J. 1995 Oct;69(4):1246-58. doi: 10.1016/S0006-3495(95)80018-4.
Confocal laser fluorescence microscopy was used to study in real time under nearly physiological conditions the equilibration and exchange characteristics of several different fluorescently labeled molecules into chemically skinned, unfixed skeletal muscle fibers of rabbit psoas. The time required for equilibration was found to vary widely from a few minutes up to several days. Specific interactions of molecules with myofibrillar structures seem to slow down equilibration significantly. Time for equilibration, therefore, cannot simply be predicted from diffusion parameters in solution. Specific interactions resulted in characteristic labeling patterns for molecules like creatine kinase (muscle type), pyruvate kinase, actin-binding IgG, and others. For the very slowly equilibrating Rh-NEM-S1, changes in affinity upon binding to actin in the absence of calcium and subsequent slow cooperative activation, beginning at the free end of the filament at the H-zone, were observed. In the presence of calcium, however, binding of Rh-NEM-S1 was homogeneous along the whole actin filament from the very beginning of equilibration. The dissociation properties of the dynamic interactions were analyzed using a chase protocol. Even molecules that bind with rather high affinity and that can be removed only by applying extreme experimental conditions like Rh-phalloidine or Rh-troponin could be displaced easily by unlabeled homologous molecules.
共聚焦激光荧光显微镜用于在接近生理条件下实时研究几种不同荧光标记分子在兔腰大肌化学去膜、未固定骨骼肌纤维中的平衡和交换特性。发现平衡所需的时间差异很大,从几分钟到几天不等。分子与肌原纤维结构的特定相互作用似乎会显著减缓平衡。因此,平衡时间不能简单地从溶液中的扩散参数预测。特定相互作用导致了肌酸激酶(肌肉型)、丙酮酸激酶、肌动蛋白结合IgG等分子的特征性标记模式。对于平衡非常缓慢的Rh-NEM-S1,观察到在没有钙的情况下与肌动蛋白结合时亲和力的变化以及随后从H区细丝自由端开始的缓慢协同激活。然而,在有钙的情况下,从平衡开始时起,Rh-NEM-S1在整个肌动蛋白丝上的结合都是均匀的。使用追踪方案分析了动态相互作用的解离特性。即使是那些以相当高的亲和力结合且只能通过应用Rh-鬼笔环肽或Rh-肌钙蛋白等极端实验条件才能去除的分子,也可以很容易地被未标记的同源分子取代。