Zhou Beifei, Hogg Philip J, Gräter Frauke
CAS-MPG Partner Institute and Key Laboratory for Computational Biology (PICB), Shanghai, China; Heidelberg Institute for Theoretical Studies, Heidelberg, Germany.
The Centenary Institute and National Health and Medical Research Council Clinical Trials Centre, University of Sydney, Sydney, Australia.
Biophys J. 2017 Jan 10;112(1):78-86. doi: 10.1016/j.bpj.2016.12.003.
Tissue factor (TF) is a transmembrane glycoprotein that plays distinct roles in the initiation of extrinsic coagulation cascade and thrombosis. TF contains two disulfide bonds, one each in the N-terminal and C-terminal extracellular domains. The C-domain disulfide, Cys186-Cys209, has a -RHStaple configuration in crystal structures, suggesting that this disulfide carries high pre-stress. The redox state of this disulfide has been proposed to regulate TF encryption/decryption. Ablating the N-domain Cys49-Cys57 disulfide bond was found to increase the redox potential of the Cys186-Cys209 bond, implying an allosteric communication between the domains. Using molecular dynamics simulations, we observed that the Cys186-Cys209 disulfide bond retained the -RHStaple configuration, whereas the Cys49-Cys57 disulfide bond fluctuated widely. The Cys186-Cys209 bond featured the typical -RHStaple disulfide properties, such as a longer S-S bond length, larger C-S-S angles, and higher bonded prestress, in comparison to the Cys49-Cys57 bond. Force distribution analysis was used to sense the subtle structural changes upon ablating the disulfide bonds, and allowed us to identify a one-way allosteric communication mechanism from the N-terminal to the C-terminal domain. We propose a force propagation pathway using a shortest-pathway algorithm, which we suggest is a useful method for searching allosteric signal transduction pathways in proteins. As a possible explanation for the pathway being one-way, we identified a pronounced lower degree of conformational fluctuation, or effectively higher stiffness, in the N-terminal domain. Thus, the changes of the rigid domain (N-terminal domain) can induce mechanical force propagation to the soft domain (C-terminal domain), but not vice versa.
组织因子(TF)是一种跨膜糖蛋白,在外源性凝血级联反应和血栓形成的起始过程中发挥着独特作用。TF含有两个二硫键,分别位于N端和C端的细胞外结构域。C结构域二硫键(Cys186-Cys209)在晶体结构中具有-RHStaple构象,表明该二硫键具有较高的预张力。有人提出该二硫键的氧化还原状态可调节TF的加密/解密。研究发现,去除N结构域的Cys49-Cys57二硫键会增加Cys186-Cys209键的氧化还原电位,这意味着结构域之间存在变构通讯。通过分子动力学模拟,我们观察到Cys186-Cys209二硫键保持-RHStaple构象,而Cys49-Cys57二硫键则波动较大。与Cys49-Cys57键相比,Cys186-Cys209键具有典型的-RHStaple二硫键特性,如较长的S-S键长度、较大的C-S-S角度和较高的键合预张力。通过力分布分析来检测去除二硫键后的细微结构变化,使我们能够识别从N端到C端结构域的单向变构通讯机制。我们使用最短路径算法提出了一种力传播途径,我们认为这是一种搜索蛋白质变构信号转导途径的有用方法。作为该途径为单向的一种可能解释,我们发现N端结构域的构象波动程度明显较低,或有效刚度较高。因此,刚性结构域(N端结构域)的变化可诱导机械力传播到柔性结构域(C端结构域),但反之则不然。