Prescott Thomas P, Lang Moritz, Papachristodoulou Antonis
Department of Engineering Science, University of Oxford, Oxford, United Kingdom; Life Sciences Interface Doctoral Training Centre, University of Oxford, Oxford, United Kingdom.
Department of Biosystems Science and Engineering, ETH Zürich, Basel, Switzerland; Swiss Institute of Bioinformatics, Basel, Switzerland.
PLoS Comput Biol. 2015 May 1;11(5):e1004235. doi: 10.1371/journal.pcbi.1004235. eCollection 2015 May.
Large, naturally evolved biomolecular networks typically fulfil multiple functions. When modelling or redesigning such systems, functional subsystems are often analysed independently first, before subsequent integration into larger-scale computational models. In the design and analysis process, it is therefore important to quantitatively analyse and predict the dynamics of the interactions between integrated subsystems; in particular, how the incremental effect of integrating a subsystem into a network depends on the existing dynamics of that network. In this paper we present a framework for simulating the contribution of any given functional subsystem when integrated together with one or more other subsystems. This is achieved through a cascaded layering of a network into functional subsystems, where each layer is defined by an appropriate subset of the reactions. We exploit symmetries in our formulation to exhaustively quantify each subsystem's incremental effects with minimal computational effort. When combining subsystems, their isolated behaviour may be amplified, attenuated, or be subject to more complicated effects. We propose the concept of mutual dynamics to quantify such nonlinear phenomena, thereby defining the incompatibility and cooperativity between all pairs of subsystems when integrated into any larger network. We exemplify our theoretical framework by analysing diverse behaviours in three dynamic models of signalling and metabolic pathways: the effect of crosstalk mechanisms on the dynamics of parallel signal transduction pathways; reciprocal side-effects between several integral feedback mechanisms and the subsystems they stabilise; and consequences of nonlinear interactions between elementary flux modes in glycolysis for metabolic engineering strategies. Our analysis shows that it is not sufficient to just specify subsystems and analyse their pairwise interactions; the environment in which the interaction takes place must also be explicitly defined. Our framework provides a natural representation of nonlinear interaction phenomena, and will therefore be an important tool for modelling large-scale evolved or synthetic biomolecular networks.
大型的、自然进化的生物分子网络通常履行多种功能。在对这类系统进行建模或重新设计时,往往先独立分析功能子系统,然后再将其整合到更大规模的计算模型中。因此,在设计和分析过程中,定量分析和预测整合后的子系统之间相互作用的动态变化非常重要;特别是将一个子系统整合到网络中的增量效应如何取决于该网络现有的动态变化。在本文中,我们提出了一个框架,用于模拟任何给定功能子系统与一个或多个其他子系统整合时的贡献。这是通过将网络级联分层为功能子系统来实现的,其中每一层由反应的适当子集定义。我们在公式中利用对称性,以最小的计算量详尽地量化每个子系统的增量效应。当组合子系统时,它们的孤立行为可能会被放大、减弱或受到更复杂的影响。我们提出相互动态的概念来量化这种非线性现象,从而定义整合到任何更大网络中的所有子系统对之间的不相容性和协同性。我们通过分析信号传导和代谢途径的三个动态模型中的不同行为来举例说明我们的理论框架:串扰机制对平行信号转导途径动态变化的影响;几个积分反馈机制与其稳定的子系统之间的相互副作用;以及糖酵解中基本通量模式之间的非线性相互作用对代谢工程策略的影响。我们的分析表明,仅仅指定子系统并分析它们的成对相互作用是不够的;相互作用发生的环境也必须明确界定。我们的框架为非线性相互作用现象提供了一种自然的表示方式,因此将成为对大规模进化或合成生物分子网络进行建模的重要工具。