Department of Chemistry, State University of New York at Stony Brook, Stony Brook, NY 11794, USA.
Phys Chem Chem Phys. 2019 Mar 6;21(10):5634-5645. doi: 10.1039/c8cp06803h.
Successful extensions of protein-folding energy landscape theory to intrinsically disordered proteins' (IDPs') binding-coupled-folding transition can enormously simplify this biomolecular process into diffusion along a limited number of reaction coordinates, and the dynamics subsequently is described by Kramers' rate theory. As the critical pre-factor, the diffusion coefficient D has direct implications on the binding kinetics. Here, we employ a structure-based model (SBM) to calculate D in the binding-folding of an IDP prototype. We identify a strong position-dependent D during binding by applying a reaction coordinate that directly measures the fluctuations in a Cartesian configuration space. Using the malleability of the SBM, we modulate the degree of conformational disorder in an isolated IDP and determine complex effects of intrinsic disorder on D varying for different binding stages. Here, D tends to increase with disorder during initial binding but shows a non-monotonic relationship with disorder in terms of a decrease-followed-by-increase in D during the late binding stage. The salt concentration, which correlates with electrostatic interactions via Debye-Hückel theory in our SBM, also modulates D in a stepwise way. The speeding up of diffusion by electrostatic interactions is observed during the formation of the encounter complex at the beginning of binding, while the last diffusive binding dynamics is hindered by non-native salt bridges. Because D describes the diffusive speed locally, which implicitly reflects the roughness of the energy landscape, we are eventually able to portray the binding energy landscape, including that from IDPs' binding, then to binding with partial folding, and finally to rigid docking, as well as that under different environmental salt concentrations. Our theoretical results provide key mechanistic insights into IDPs' binding-folding, which is internally conformation- and externally salt-controlled with respect to diffusion.
成功地将蛋白质折叠能景理论扩展到固有无序蛋白质(IDP)的结合偶联折叠转变,可以将这个生物分子过程极大地简化为沿着有限数量的反应坐标扩散,随后动力学由克拉默斯速率理论描述。作为关键的前置因子,扩散系数 D 直接影响结合动力学。在这里,我们使用基于结构的模型(SBM)来计算 IDP 原型结合折叠中的 D。我们通过应用直接测量笛卡尔构象空间波动的反应坐标,确定了结合过程中强烈的位置相关 D。利用 SBM 的可变形性,我们在孤立的 IDP 中调节构象无序的程度,并确定固有无序对不同结合阶段 D 的复杂影响。在这里,D 在初始结合过程中随着无序程度的增加而增加,但在结合后期,D 与无序程度呈非单调关系,先减少后增加。盐浓度通过我们的 SBM 中的德拜-休克尔理论与静电相互作用相关,以逐步的方式调节 D。在结合开始时形成遭遇复合物期间,静电相互作用加速了扩散,而最后扩散结合动力学则受到非天然盐桥的阻碍。由于 D 描述了局部的扩散速度,隐含地反映了能景的粗糙度,我们最终能够描绘结合能景,包括 IDP 的结合、部分折叠的结合和刚性对接的结合,以及在不同环境盐浓度下的结合。我们的理论结果为 IDP 结合折叠提供了关键的机制见解,结合折叠过程是内部构象和外部盐控制的扩散过程。