Department of Biological Sciences, University of Alberta, Edmonton, AB, Canada.
Department of Mechanical Engineering, University of Alberta, Edmonton, AB, Canada.
PLoS One. 2021 Feb 26;16(2):e0247684. doi: 10.1371/journal.pone.0247684. eCollection 2021.
Superoxide dismutase 1 (SOD1) is known to be involved in the pathogenesis of Amyotrophic Lateral Sclerosis (ALS) and is therefore considered to be an important ALS drug target. Identifying potential drug leads that bind to SOD1 and characterizing their interactions by nuclear magnetic resonance (NMR) spectroscopy is complicated by the fact that SOD1 is a homodimer. Creating a monomeric version of SOD1 could alleviate these issues. A specially designed monomeric form of human superoxide dismutase (T2M4SOD1) was cloned into E. coli and its expression significantly enhanced using a number of novel DNA sequence, leader peptide and growth condition optimizations. Uniformly 15N-labeled T2M4SOD1 was prepared from minimal media using 15NH4Cl as the 15N source. The T2M4SOD1 monomer (both 15N labeled and unlabeled) was correctly folded as confirmed by 1H-NMR spectroscopy and active as confirmed by an in-gel enzymatic assay. To demonstrate the utility of this new SOD1 expression system for NMR-based drug screening, eight pyrimidine compounds were tested for binding to T2M4SOD1 by monitoring changes in their 1H NMR and/or 19F-NMR spectra. Weak binding to 5-fluorouridine (FUrd) was observed via line broadening, but very minimal spectral changes were seen with uridine, 5-bromouridine or trifluridine. On the other hand, 1H-NMR spectra of T2M4SOD1 with uracil or three halogenated derivatives of uracil changed dramatically suggesting that the pyrimidine moiety is the crucial binding component of FUrd. Interestingly, no change in tryptophan 32 (Trp32), the putative receptor for FUrd, was detected in the 15N-NMR spectra of 15N-T2M4SOD1 when mixed with these uracil analogs. Molecular docking and molecular dynamic (MD) studies indicate that interaction with Trp32 of SOD1 is predicted to be weak and that there was hydrogen bonding with the nearby aspartate (Asp96), potentiating the Trp32-uracil interaction. These studies demonstrate that monomeric T2M4SOD1 can be readily used to explore small molecule interactions via NMR.
超氧化物歧化酶 1(SOD1)已知参与肌萎缩侧索硬化症(ALS)的发病机制,因此被认为是 ALS 的重要药物靶点。通过核磁共振(NMR)光谱鉴定与 SOD1 结合的潜在药物先导化合物并表征其相互作用,由于 SOD1 是同源二聚体,因此变得复杂。创建 SOD1 的单体版本可以缓解这些问题。一种专门设计的人超氧化物歧化酶(T2M4SOD1)单体形式被克隆到大肠杆菌中,并通过使用多种新型 DNA 序列、前导肽和生长条件优化来显著增强其表达。使用 15NH4Cl 作为 15N 源,从最小培养基中制备均匀标记的 15N-T2M4SOD1。通过 1H-NMR 光谱证实 T2M4SOD1 单体(标记和未标记的 15N)正确折叠,并通过凝胶内酶测定证实其具有活性。为了证明这种新的 SOD1 表达系统在基于 NMR 的药物筛选中的实用性,通过监测其 1H NMR 和/或 19F-NMR 光谱的变化,测试了八种嘧啶化合物与 T2M4SOD1 的结合情况。通过线宽变宽观察到与 5-氟尿嘧啶(FUrd)的弱结合,但与尿嘧啶、5-溴尿嘧啶或三氟尿嘧啶观察到非常小的光谱变化。另一方面,与尿嘧啶或嘧啶环上三个卤素取代的衍生物的 T2M4SOD1 的 1H-NMR 光谱发生了剧烈变化,表明嘧啶部分是 FUrd 的关键结合成分。有趣的是,在与这些尿嘧啶类似物混合时,未检测到 15N-T2M4SOD1 的 15N-NMR 光谱中色氨酸 32(Trp32)的变化,Trp32 是 FUrd 的假定受体。分子对接和分子动力学(MD)研究表明,SOD1 与 Trp32 的相互作用预计较弱,并且与附近的天冬氨酸(Asp96)形成氢键,增强了 Trp32-尿嘧啶相互作用。这些研究表明,单体 T2M4SOD1 可以通过 NMR 轻松用于探索小分子相互作用。