Gaertner A, Wegner A
Institute of Physiological Chemistry, Ruhr-University Bochum, FRG.
J Muscle Res Cell Motil. 1991 Feb;12(1):27-36. doi: 10.1007/BF01781171.
Insertin, a protein purified from chicken gizzard smooth muscle, has been shown to retard but not to inhibit actin polymerization at the barbed ends of actin filaments. This effect has been explained by a model in which insertin remains bound to the barbed ends of actin filaments and new actin molecules are inserted into filaments between the barbed ends and barbed end-bound insertin molecules. In this paper we discuss the mechanism of the insertion reaction on a molecular level. A number of simple models were devised and were judged by their agreement with available experimental data. In one class of models insertin was assumed to dissociate from filament ends and to re-associate with the ends. Actin monomers would then bind to a filament end between a dissociation and an association reaction of insertin. In one of the two proposed models in this class insertin binds to an ATP-containing terminal subunit with higher affinity than to an ADP-containing terminal subunit. Dissociation of insertin is brought about by ATP hydrolysis at the terminal filament subunit. Insertion was then thought to re-associate with a filament end following binding of an ATP-containing actin monomer to the filament end. In the other of the two models' insertin was assumed to occur in two conformations which bind to filament ends with different affinities. Association and dissociation of insertin is caused by interconversion between the two forms of insertin. Both models turned out to be incompatible with experimental data. All types of models in which retardation of actin polymerization is brought about by dissociation and re-association of insertin with filament ends can be excluded by a common argument. As 10 nM insertin retards polymerization of 2 microns monomeric actin with maximal efficiency, the rate constant of binding of insertin to a filament end must be considerably higher (greater than 2 microM/10 nM = 200-fold). As the rate of association of actin with a barbed end is almost diffusion-controlled, assembly of insertin with a filament end would have to exceed the rate of a diffusion-controlled reaction. In the other class of models it was assumed that insertin remains permanently bound to filament ends during association or dissociation of an actin molecule and to move towards the terminal subunit of filaments. These models are compatible with experimental data. Thus, models are favoured where insertin remains bound to filament ends during polymerization and depolymerization of actin.
插入蛋白是一种从鸡胗平滑肌中纯化得到的蛋白质,已被证明能延缓但不能抑制肌动蛋白丝在其带刺末端的聚合。这种效应已通过一个模型得到解释,在该模型中,插入蛋白保持与肌动蛋白丝的带刺末端结合,新的肌动蛋白分子被插入到带刺末端与结合在带刺末端的插入蛋白分子之间的丝中。在本文中,我们在分子水平上讨论插入反应的机制。设计了许多简单模型,并根据它们与现有实验数据的一致性来判断。在一类模型中,假定插入蛋白从丝末端解离并重新与末端结合。然后肌动蛋白单体将在插入蛋白的解离和结合反应之间与丝末端结合。在这类模型中提出的两个模型之一中,插入蛋白与含ATP的末端亚基结合的亲和力高于与含ADP的末端亚基结合的亲和力。插入蛋白的解离是由丝末端亚基处的ATP水解引起的。然后认为在含ATP的肌动蛋白单体与丝末端结合后,插入蛋白重新与丝末端结合。在两个模型中的另一个模型中,假定插入蛋白以两种构象存在,这两种构象以不同的亲和力与丝末端结合。插入蛋白的结合和解离是由插入蛋白的两种形式之间的相互转化引起的。事实证明这两个模型都与实验数据不相符。所有通过插入蛋白与丝末端的解离和重新结合来导致肌动蛋白聚合延缓的模型类型都可以通过一个共同的论点被排除。由于10 nM的插入蛋白能以最大效率延缓2微米单体肌动蛋白的聚合,插入蛋白与丝末端结合的速率常数必须相当高(大于2 microM/10 nM = 200倍)。由于肌动蛋白与带刺末端的结合速率几乎是扩散控制的,插入蛋白与丝末端的组装速率将不得不超过扩散控制反应的速率。在另一类模型中,假定在肌动蛋白分子的结合或解离过程中,插入蛋白始终与丝末端结合并向丝的末端亚基移动。这些模型与实验数据相符。因此,倾向于采用在肌动蛋白聚合和解聚过程中插入蛋白始终与丝末端结合的模型。