Flynn Terence C, Swint-Kruse Liskin, Kong Yifei, Booth Christopher, Matthews Kathleen S, Ma Jianpeng
Department of Bioengineering, Rice University, Houston, Texas 77005, USA.
Protein Sci. 2003 Nov;12(11):2523-41. doi: 10.1110/ps.03188303.
The crystal structures of lactose repressor protein (LacI) provide static endpoint views of the allosteric transition between DNA- and IPTG-bound states. To obtain an atom-by-atom description of the pathway between these two conformations, motions were simulated with targeted molecular dynamics (TMD). Strikingly, this homodimer exhibited asymmetric dynamics. All asymmetries observed in this simulation are reproducible and can begin on either of the two monomers. Asymmetry in the simulation originates around D149 and was traced back to the pre-TMD equilibrations of both conformations. In particular, hydrogen bonds between D149 and S193 adopt a variety of configurations during repetitions of this process. Changes in this region propagate through the structure via noncovalent interactions of three interconnected pathways. The changes of pathway 1 occur first on one monomer. Alterations move from the inducer-binding pocket, through the N-subdomain beta-sheet, to a hydrophobic cluster at the top of this region and then to the same cluster on the second monomer. These motions result in changes at (1) side chains that form an interface with the DNA-binding domains and (2) K84 and K84', which participate in the monomer-monomer interface. Pathway 2 reflects consequent reorganization across this subunit interface, most notably formation of a H74-H74rsquo; pi-stacking intermediate. Pathway 3 extends from the rear of the inducer-binding pocket, across a hydrogen-bond network at the bottom of the pocket, and transverses the monomer-monomer interface via changes in H74 and H74rsquo;. In general, intermediates detected in this study are not apparent in the crystal structures. Observations from the simulations are in good agreement with biochemical data and provide a spatial and sequential framework for interpreting existing genetic data.
乳糖阻遏蛋白(LacI)的晶体结构提供了DNA结合状态和异丙基-β-D-硫代半乳糖苷(IPTG)结合状态之间变构转变的静态终点视图。为了获得这两种构象之间路径的逐个原子描述,使用靶向分子动力学(TMD)模拟了运动。引人注目的是,这种同型二聚体表现出不对称动力学。在该模拟中观察到的所有不对称都是可重复的,并且可以在两个单体中的任何一个上开始。模拟中的不对称起源于D149周围,并追溯到两种构象的TMD预平衡。特别是,D149和S193之间的氢键在该过程的重复中采用了多种构型。该区域的变化通过三条相互连接的途径的非共价相互作用在结构中传播。途径1的变化首先发生在一个单体上。改变从诱导剂结合口袋开始,通过N亚结构域β-折叠,到达该区域顶部的疏水簇,然后到达第二个单体上的相同簇。这些运动导致(1)与DNA结合结构域形成界面的侧链和(2)参与单体-单体界面的K84和K84'发生变化。途径2反映了整个亚基界面随之而来的重组,最显著的是形成了H74-H74'π堆积中间体。途径3从诱导剂结合口袋的后部延伸,穿过口袋底部的氢键网络,并通过H74和H74'的变化横穿单体-单体界面。一般来说,在本研究中检测到的中间体在晶体结构中并不明显。模拟结果与生化数据非常吻合,并为解释现有遗传数据提供了一个空间和序列框架。