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Molecular mechanism of cutokinesis

细胞运动的分子机制

基本信息

批准号：
59490013
负责人：
MABUCHI Issei
金额：
$ 6.02万
依托单位：
University of Tokyo
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1984
资助国家：
日本
起止时间：
1984 至 1986
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-59490013/
关键词：
Cytokinesis Actin Actin-modulating Proteins 収縮環

项目摘要

The purpose of this research project has been to clarify the mechanism of cytokinesis at a molecular level. The first approach we used was to study the formation of the contractile ring. As a result, we found following seven actin-modulating proteins and characterized them. (1) 45K protein-actin complex which is able to modulate both the rate of polymerization of actin and the end-to-end interactions of actin filaments by binding to the barbed end of the actin filament. (2) Alpha-actinin which crosslinks actin filaments in the absence of calcium ions to form filament bundles. (3) 100K protein which severs actin filaments in the presence of calcium ions. (4) 250K protein which crosslinks actin filaments in a Ca-independent manner. (5) 20K protein-actin complex which has prpperties similar to the 45K protein-actin complex. This protein was thought to attach to the inner surface of the plasma membrane and link actin filaments to the membrane. (6) Spectrin which crosslinks actin fialments in a Ca-independent manner. (7) A Ca-binding 15K protein which inhibits the rate of actin polymerization as well as microtubule assembly. Among these proteins, alpha-actinin was labeled with a fluorescent reagent and microinjected into living egg and pursued its movement in the cell. It was concentrated in the cleavage furrow region at cytokinesis. Therefore, this protein may be relevant to cytokinesis.The second approach was to study the mechanism of contraction of the cleavage furrow using cleavage furrow isolated from newt egg. By using electron microscopy we demonstrated that the parallel actin filaments in the contractile arc were crosslinked by various actin-crosslinking proteins. We also demonstrated that the contraction could be induced in the isolated furrow in vitro and it was inhibited by actin inhibitors.

该研究项目的目的是在分子水平上阐明胞质分裂的机制。我们使用的第一种方法是研究收缩环的形成。结果，我们发现了以下七种肌动蛋白调节蛋白并对其进行了表征。 (1) 45K 蛋白质-肌动蛋白复合物，能够通过与肌动蛋白丝的倒刺末端结合来调节肌动蛋白的聚合速率和肌动蛋白丝的端到端相互作用。 (2) α-肌动蛋白，在没有钙离子的情况下交联肌动蛋白丝形成丝束。 (3) 100K 蛋白质，在钙离子存在的情况下切断肌动蛋白丝。 (4) 250K 蛋白质，以不依赖 Ca 的方式交联肌动蛋白丝。 (5)20K蛋白-肌动蛋白复合物，其性质与45K蛋白-肌动蛋白复合物相似。这种蛋白质被认为附着在质膜的内表面并将肌动蛋白丝连接到膜上。 (6)血影蛋白，其以不依赖于Ca的方式交联肌动蛋白细丝。 (7) 一种 Ca 结合 15K 蛋白，可抑制肌动蛋白聚合和微管组装的速率。在这些蛋白质中，α-肌动蛋白被荧光试剂标记并显微注射到活卵中并追踪其在细胞中的运动。它集中在胞质分裂时的卵裂沟区域。因此，该蛋白可能与胞质分裂有关。第二种方法是利用从蝾螈卵中分离的卵裂沟来研究卵裂沟的收缩机制。通过使用电子显微镜，我们证明收缩弧中的平行肌动蛋白丝被各种肌动蛋白交联蛋白交联。我们还证明，在体外分离的沟中可以诱导收缩，并且可以被肌动蛋白抑制剂抑制。