Schreiner G F, Unanue E R
J Exp Med. 1976 Jan 1;143(1):15-31. doi: 10.1084/jem.143.1.15.
Capping of anti-Ig-Ig complexes was studied in murine B lymphocytes. Morphological studies indicated that caps formed rapidly on cells before any changes in shape. The first changes in cell shape were evident as a contraction right under the cap area. The removal of extracellular calcium had no effect on cap formation. Furthermore, the introduction of calcium by the ionophore A-23187 stopped capping. The ionophere by itself in the absence of extracellular calcium had no effect. Caps were found to be disrupted, the complexes scattering over the entire cell surface if the cells were treated by A-23187 after the caps had formed. The disruptive effect of A-23187 as dependent on extracellular calcium and could be stopped by drugs that affected energy metabolism. The cytochalasins also disrupted the formed caps. Drugs that affect energy metabolism by themselves did not disrupt the caps. We interpret the effects of the ionophore as resulting from a systemic hypercontractility of microfilaments. A theory for explaining the formation and disruption of capping is discussed.
在小鼠B淋巴细胞中研究了抗Ig-Ig复合物的帽化现象。形态学研究表明,在细胞形状发生任何变化之前,帽在细胞上迅速形成。细胞形状的最初变化表现为帽区域正下方的收缩。去除细胞外钙对帽的形成没有影响。此外,通过离子载体A-23187引入钙会阻止帽化。在没有细胞外钙的情况下,离子载体本身没有作用。如果在帽形成后用A-23187处理细胞,会发现帽被破坏,复合物分散在整个细胞表面。A-23187的破坏作用依赖于细胞外钙,并且可以被影响能量代谢的药物阻止。细胞松弛素也会破坏已形成的帽。本身影响能量代谢的药物不会破坏帽。我们将离子载体的作用解释为微丝系统性过度收缩的结果。讨论了一种解释帽化形成和破坏的理论。