Biophysical Sciences Institute, Durham University, Durham, United Kingdom ; Department of Chemistry, Durham University, Durham, United Kingdom.
PLoS Biol. 2013 Sep;11(9):e1001651. doi: 10.1371/journal.pbio.1001651. Epub 2013 Sep 10.
Allostery is a fundamental process by which ligand binding to a protein alters its activity at a distinct site. There is growing evidence that allosteric cooperativity can be communicated by modulation of protein dynamics without conformational change. The mechanisms, however, for communicating dynamic fluctuations between sites are debated. We provide a foundational theory for how allostery can occur as a function of low-frequency dynamics without a change in structure. We have generated coarse-grained models that describe the protein backbone motions of the CRP/FNR family transcription factors, CAP of Escherichia coli and GlxR of Corynebacterium glutamicum. The latter we demonstrate as a new exemplar for allostery without conformation change. We observe that binding the first molecule of cAMP ligand is correlated with modulation of the global normal modes and negative cooperativity for binding the second cAMP ligand without a change in mean structure. The theory makes key experimental predictions that are tested through an analysis of variant proteins by structural biology and isothermal calorimetry. Quantifying allostery as a free energy landscape revealed a protein "design space" that identified the inter- and intramolecular regulatory parameters that frame CRP/FNR family allostery. Furthermore, through analyzing CAP variants from diverse species, we demonstrate an evolutionary selection pressure to conserve residues crucial for allosteric control. This finding provides a link between the position of CRP/FNR transcription factors within the allosteric free energy landscapes and evolutionary selection pressures. Our study therefore reveals significant features of the mechanistic basis for allostery. Changes in low-frequency dynamics correlate with allosteric effects on ligand binding without the requirement for a defined spatial pathway. In addition to evolving suitable three-dimensional structures, CRP/FNR family transcription factors have been selected to occupy a dynamic space that fine-tunes biological activity and thus establishes the means to engineer allosteric mechanisms driven by low-frequency dynamics.
变构作用是一种基本过程,通过这种过程,配体与蛋白质的结合会改变其在特定部位的活性。越来越多的证据表明,变构协同作用可以通过调节蛋白质动力学而无需构象变化来传递。然而,关于在不同部位之间传递动态波动的机制仍存在争议。我们提供了一种基础理论,说明变构作用如何在没有结构变化的情况下作为低频动力学的函数发生。我们已经生成了粗粒化模型,这些模型描述了 CRP/FNR 家族转录因子、大肠杆菌的 CAP 和谷氨酸棒杆菌的 GlxR 的蛋白质骨架运动。我们证明后者是没有构象变化的变构作用的新范例。我们观察到,结合第一个 cAMP 配体分子与全局正常模式的调制相关,并且在不改变平均结构的情况下,第二个 cAMP 配体的结合具有负协同性。该理论做出了关键的实验预测,这些预测通过结构生物学和等温量热法对变体蛋白的分析进行了检验。通过将变构作用量化为自由能景观,揭示了一种蛋白质“设计空间”,该空间确定了 CRP/FNR 家族变构作用的分子内和分子间调节参数。此外,通过分析来自不同物种的 CAP 变体,我们证明了进化选择压力来保守变构控制的关键残基。这一发现为 CRP/FNR 转录因子在变构自由能景观中的位置与进化选择压力之间提供了联系。因此,我们的研究揭示了变构作用的机制基础的重要特征。低频动力学的变化与配体结合的变构效应相关,而无需明确的空间途径。除了进化出合适的三维结构外,CRP/FNR 家族转录因子还被选择占据动态空间,从而微调生物活性,从而建立了由低频动力学驱动的变构机制的设计手段。