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肌动蛋白聚合。细胞松弛素D的作用机制。

Actin polymerization. The mechanism of action of cytochalasin D.

作者信息

Goddette D W, Frieden C

出版信息

J Biol Chem. 1986 Dec 5;261(34):15974-80.

PMID:3023337
Abstract

Fluorescence changes using actin covalently labeled with N-(1-pyrenyl)iodoacetamide have been used to determine the effect of cytochalasin D on actin polymerization. A mechanism for the effect of cytochalasin D on actin polymerization is presented, which explains the experimental observation of a cytochalasin D-induced increase in the initial rate of polymerization and a decrease in the final extent of the reaction. Central to this mechanism is the Mg2+-dependent formation of cytochalasin D-induced dimers. The dimers serve as nuclei to enhance the polymerization rate. Binding of Mg2+ to a low affinity site on the dimer induces a conformational change which can be observed as a rapid fluorescence increase. A subsequent time-dependent fluorescence decrease observed prior to polymerization appears to represent ATP hydrolysis resulting in dissociation of the dimer and release of actin monomers containing ADP. We postulate that a slow rate of exchange of ATP for bound ADP relative to hydrolysis results in the accumulation of monomers containing ADP. As these monomers have a high critical concentration, the final extent of polymerization is reduced dramatically. The Mg2+ dependence of the final extent of polymerization in the presence of cytochalasin D is also explained in the context of this mechanism.

摘要

利用用N-(1-芘基)碘乙酰胺共价标记的肌动蛋白的荧光变化来确定细胞松弛素D对肌动蛋白聚合的影响。本文提出了细胞松弛素D对肌动蛋白聚合作用的机制,该机制解释了细胞松弛素D诱导聚合初始速率增加和反应最终程度降低的实验观察结果。该机制的核心是细胞松弛素D诱导的二聚体的Mg2+依赖性形成。这些二聚体作为核来提高聚合速率。Mg2+与二聚体上的低亲和力位点结合会诱导构象变化,这可表现为荧光快速增加。在聚合之前观察到的随后的时间依赖性荧光降低似乎代表ATP水解,导致二聚体解离并释放含有ADP的肌动蛋白单体。我们推测,相对于水解而言,ATP与结合的ADP的交换速率较慢导致含有ADP的单体积累。由于这些单体具有高临界浓度,聚合的最终程度会显著降低。在该机制的背景下,也解释了在细胞松弛素D存在下聚合最终程度对Mg2+的依赖性。

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