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变形虫趋化运动过程中的肌动蛋白聚合和伪足延伸。

Actin polymerization and pseudopod extension during amoeboid chemotaxis.

作者信息

Condeelis J, Hall A, Bresnick A, Warren V, Hock R, Bennett H, Ogihara S

机构信息

Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, NY 10461.

出版信息

Cell Motil Cytoskeleton. 1988;10(1-2):77-90. doi: 10.1002/cm.970100113.

DOI:10.1002/cm.970100113
PMID:3052871
Abstract

Amoebae of the cellular slime mold Dictyostelium discoideum are an excellent model system for the study of amoeboid chemotaxis. These cells can be studied as a homogeneous population whose response to chemotactic stimulation is sufficiently synchronous to permit the correlation of the changes in cell shape and biochemical events during chemotaxis. Having demonstrated this synchrony of response, we show that actin polymerization occurs in two stages during stimulation with chemoattractants. The assembly of F-actin that peaks between 40 and 60 sec after the onset of stimulation is temporally correlated with the growth of new pseudopods. F-actin, which is assembled by 60 sec after stimulation begins, is localized in the new pseudopods that are extended at this time. Both stages of actin polymerization during chemotactic stimulation involve polymerization at the barbed ends of actin filaments based on the cytochalasin sensitivity of this response. We present a hypothesis in which actin polymerization is one of the major driving forces for pseudopod extension during chemotaxis. The predictions of this model, that localized regulation of actin nucleation activity and actin filament cross-linking must occur, are discussed in the context of current models for signal transduction and of recent information regarding the types of actin-binding proteins that are present in the cell cortex.

摘要

细胞黏菌盘基网柄菌的变形虫是研究变形虫趋化性的优秀模型系统。这些细胞可以作为一个同质群体进行研究,其对趋化刺激的反应足够同步,能够使趋化过程中细胞形状变化与生化事件相互关联。在证明了这种反应的同步性之后,我们发现在用趋化因子刺激过程中,肌动蛋白聚合发生在两个阶段。刺激开始后40到60秒之间达到峰值的F-肌动蛋白组装在时间上与新伪足的生长相关。刺激开始后60秒内组装的F-肌动蛋白定位于此时延伸的新伪足中。基于这种反应对细胞松弛素的敏感性,趋化刺激过程中肌动蛋白聚合的两个阶段都涉及肌动蛋白丝的刺端聚合。我们提出了一个假说,即肌动蛋白聚合是趋化过程中伪足延伸的主要驱动力之一。该模型的预测,即必须发生肌动蛋白成核活性和肌动蛋白丝交联的局部调节,将在当前信号转导模型以及关于细胞皮层中存在的肌动蛋白结合蛋白类型的最新信息的背景下进行讨论。

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