Galkin Vitold E, Orlova Albina, Cherepanova Olga, Lebart Marie-Christine, Egelman Edward H
Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, VA 22908-0733, USA.
Proc Natl Acad Sci U S A. 2008 Feb 5;105(5):1494-8. doi: 10.1073/pnas.0708667105. Epub 2008 Jan 30.
Many actin binding proteins have a modular architecture, and calponin-homology (CH) domains are one such structurally conserved module found in numerous proteins that interact with F-actin. The manner in which CH-domains bind F-actin has been controversial. Using cryo-EM and a single-particle approach to helical reconstruction, we have generated 12-A-resolution maps of F-actin alone and F-actin decorated with a fragment of human fimbrin (L-plastin) containing tandem CH-domains. The high resolution allows an unambiguous fit of the crystal structure of fimbrin into the map. The interaction between fimbrin ABD2 (actin binding domain 2) and F-actin is different from any interaction previously observed or proposed for tandem CH-domain proteins, showing that the structural conservation of the CH-domains does not lead to a conserved mode of interaction with F-actin. Both the stapling of adjacent actin protomers and the additional closure of the nucleotide binding cleft in F-actin when the fimbrin fragment binds may explain how fimbrin can stabilize actin filaments. A mechanism is proposed where ABD1 of fimbrin becomes activated for binding a second actin filament after ABD2 is bound to a first filament, and this can explain how mutations of residues buried in the interface between ABD2 and ABD1 can rescue temperature-sensitive defects in actin.
许多肌动蛋白结合蛋白具有模块化结构,而钙调蛋白同源(CH)结构域就是众多与F-肌动蛋白相互作用的蛋白质中发现的一种结构保守的模块。CH结构域与F-肌动蛋白结合的方式一直存在争议。我们利用冷冻电镜和单颗粒方法进行螺旋重建,生成了单独的F-肌动蛋白以及用含有串联CH结构域的人丝束蛋白(L- plastin)片段修饰的F-肌动蛋白的12埃分辨率图谱。高分辨率使得丝束蛋白的晶体结构能够明确地拟合到图谱中。丝束蛋白ABD2(肌动蛋白结合结构域2)与F-肌动蛋白之间的相互作用不同于先前观察到的或针对串联CH结构域蛋白所提出的任何相互作用,这表明CH结构域的结构保守性并不导致与F-肌动蛋白相互作用的保守模式。当丝束蛋白片段结合时,相邻肌动蛋白原纤维的钉扎以及F-肌动蛋白中核苷酸结合裂隙的额外闭合可能解释了丝束蛋白如何稳定肌动蛋白丝。我们提出了一种机制,即丝束蛋白的ABD1在ABD2与第一根肌动蛋白丝结合后被激活以结合第二根肌动蛋白丝,这可以解释ABD2与ABD1之间界面处埋藏的残基突变如何挽救肌动蛋白中的温度敏感缺陷。