Department of Biomedical Engineering and Institute for Computational Medicine, Johns Hopkins University, Baltimore, MD.
Department of Environmental Toxicology, University of California Santa Cruz, Santa Cruz, CA.
Mol Biol Evol. 2018 Jun 1;35(6):1507-1519. doi: 10.1093/molbev/msy036.
The evolution of new biochemical activities frequently involves complex dependencies between mutations and rapid evolutionary radiation. Mutation co-occurrence and covariation have previously been used to identify compensating mutations that are the result of physical contacts and preserve protein function and fold. Here, we model pairwise functional dependencies and higher order interactions that enable evolution of new protein functions. We use a network model to find complex dependencies between mutations resulting from evolutionary trade-offs and pleiotropic effects. We present a method to construct these networks and to identify functionally interacting mutations in both extant and reconstructed ancestral sequences (Network Analysis of Protein Adaptation). The time ordering of mutations can be incorporated into the networks through phylogenetic reconstruction. We apply NAPA to three distantly homologous β-lactamase protein clusters (TEM, CTX-M-3, and OXA-51), each of which has experienced recent evolutionary radiation under substantially different selective pressures. By analyzing the network properties of each protein cluster, we identify key adaptive mutations, positive pairwise interactions, different adaptive solutions to the same selective pressure, and complex evolutionary trajectories likely to increase protein fitness. We also present evidence that incorporating information from phylogenetic reconstruction and ancestral sequence inference can reduce the number of spurious links in the network, whereas preserving overall network community structure. The analysis does not require structural or biochemical data. In contrast to function-preserving mutation dependencies, which are frequently from structural contacts, gain-of-function mutation dependencies are most commonly between residues distal in protein structure.
新生物化学活性的进化通常涉及突变之间的复杂依赖性和快速的进化辐射。突变共发生和共变以前被用来识别补偿突变,这些突变是物理接触的结果,保留了蛋白质的功能和折叠。在这里,我们构建了模型,用于研究导致进化权衡和多效性效应的突变之间的功能依赖性和更高阶的相互作用。我们使用网络模型来发现进化权衡和多效性效应中突变之间的复杂依赖性。我们提出了一种构建这些网络的方法,并在现存和重建的祖先序列中识别功能相互作用的突变(蛋白质适应的网络分析)。通过系统发育重建,可以将突变的时间顺序纳入网络中。我们将 NAPA 应用于三个远同源的β-内酰胺酶蛋白簇(TEM、CTX-M-3 和 OXA-51),每个蛋白簇都经历了近期的进化辐射,这些辐射受到了不同的选择压力。通过分析每个蛋白簇的网络属性,我们确定了关键的适应性突变、阳性的成对相互作用、对同一选择压力的不同适应性解决方案,以及可能增加蛋白质适应性的复杂进化轨迹。我们还提供了证据表明,从系统发育重建和祖先序列推断中整合信息可以减少网络中虚假链接的数量,同时保留网络整体社区结构。该分析不需要结构或生化数据。与功能保持突变依赖性不同,功能获得突变依赖性最常见于蛋白质结构中远距离的残基之间。