Department of Chemistry and Applied Biosciences, ETH Zurich, Vladimir-Prelog-Weg 2, Zurich, 8093, Switzerland.
TUM School of Natural Sciences, Department Biosciences, Theoretical Biophysics (T38), Center for Functional Protein Assemblies (CPA), Technical University Munich (TUM), Ernst-Otto-Fischer Str. 8, Garching, 85748, Germany.
Commun Biol. 2024 Jul 24;7(1):895. doi: 10.1038/s42003-024-06575-x.
Staphylococcus aureus signal peptidase IB (SpsB) is an essential enzyme for protein secretion. While inhibition of its activity by small molecules is a well-precedented mechanism to kill bacteria, the mode of activation is however less understood. We here investigate the activation mechanism of a recently introduced activator, the antibiotic compound PK150, and demonstrate by combined experimental and Molecular Dynamics (MD) simulation studies a unique principle of enzyme stimulation. Mass spectrometric studies with an affinity-based probe of PK150 unravel the binding site of PK150 in SpsB which is used as a starting point for MD simulations. Our model shows the localization of the molecule in an allosteric pocket next to the active site which shields the catalytic dyad from excess water that destabilizes the catalytic geometry. This mechanism is validated by the placement of mutations aligning the binding pocket of PK150. While the mutants retain turnover of the SpsB substrate, no stimulation of activity is observed upon PK150 addition. Overall, our study elucidates a previously little investigated mechanism of enzyme activation and serves as a starting point for the development of future enzyme activators.
金黄色葡萄球菌信号肽酶 IB(SpsB)是一种蛋白质分泌所必需的酶。虽然通过小分子抑制其活性是一种被广泛研究的杀死细菌的机制,但酶的激活模式却知之甚少。在这里,我们研究了一种新引入的激活剂抗生素化合物 PK150 的激活机制,并通过结合实验和分子动力学(MD)模拟研究证明了一种独特的酶刺激原理。使用基于亲和性的 PK150 探针进行的质谱研究揭示了 PK150 在 SpsB 中的结合位点,该结合位点被用作 MD 模拟的起点。我们的模型显示,该分子定位于紧邻活性位点的别构口袋中,该口袋将催化二联体与过多的水隔离开来,从而破坏了催化几何形状的稳定性。通过放置与 PK150 结合口袋对齐的突变来验证该机制。虽然突变体保留了 SpsB 底物的周转,但在添加 PK150 时没有观察到活性的刺激。总的来说,我们的研究阐明了一种以前研究较少的酶激活机制,并为未来酶激活剂的开发提供了一个起点。