Murabito Ettore, Verma Malkhey, Bekker Martijn, Bellomo Domenico, Westerhoff Hans V, Teusink Bas, Steuer Ralf
Manchester Institute of Biotechnology, School of Chemical Engineering and Analytical Sciences (CEAS), Manchester Centre for Integrative Systems Biology (MCISB), The University of Manchester, Manchester, United Kingdom.
Molecular Microbial Physiology, Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, The Netherlands.
PLoS One. 2014 Sep 30;9(9):e106453. doi: 10.1371/journal.pone.0106453. eCollection 2014.
Metabolic pathways are complex dynamic systems whose response to perturbations and environmental challenges are governed by multiple interdependencies between enzyme properties, reactions rates, and substrate levels. Understanding the dynamics arising from such a network can be greatly enhanced by the construction of a computational model that embodies the properties of the respective system. Such models aim to incorporate mechanistic details of cellular interactions to mimic the temporal behavior of the biochemical reaction system and usually require substantial knowledge of kinetic parameters to allow meaningful conclusions. Several approaches have been suggested to overcome the severe data requirements of kinetic modeling, including the use of approximative kinetics and Monte-Carlo sampling of reaction parameters. In this work, we employ a probabilistic approach to study the response of a complex metabolic system, the central metabolism of the lactic acid bacterium Lactococcus lactis, subject to perturbations and brief periods of starvation. Supplementing existing methodologies, we show that it is possible to acquire a detailed understanding of the control properties of a corresponding metabolic pathway model that is directly based on experimental observations. In particular, we delineate the role of enzymatic regulation to maintain metabolic stability and metabolic recovery after periods of starvation. It is shown that the feedforward activation of the pyruvate kinase by fructose-1,6-bisphosphate qualitatively alters the bifurcation structure of the corresponding pathway model, indicating a crucial role of enzymatic regulation to prevent metabolic collapse for low external concentrations of glucose. We argue that similar probabilistic methodologies will help our understanding of dynamic properties of small-, medium- and large-scale metabolic networks models.
代谢途径是复杂的动态系统,其对扰动和环境挑战的响应由酶特性、反应速率和底物水平之间的多种相互依赖性所支配。通过构建体现相应系统特性的计算模型,可以极大地增强对这种网络产生的动态的理解。此类模型旨在纳入细胞相互作用的机制细节,以模拟生化反应系统的时间行为,并且通常需要大量动力学参数知识才能得出有意义的结论。已经提出了几种方法来克服动力学建模对数据的严格要求,包括使用近似动力学和反应参数的蒙特卡罗采样。在这项工作中,我们采用概率方法来研究复杂代谢系统(乳酸乳球菌的中心代谢)在受到扰动和短暂饥饿期时的响应。作为对现有方法的补充,我们表明有可能直接基于实验观察对相应代谢途径模型的控制特性获得详细理解。特别是,我们阐述了酶调节在维持饥饿期后的代谢稳定性和代谢恢复中的作用。结果表明,果糖 -1,6-二磷酸对丙酮酸激酶的前馈激活定性地改变了相应途径模型的分叉结构,这表明酶调节对于防止低外部葡萄糖浓度下的代谢崩溃起着关键作用。我们认为类似的概率方法将有助于我们理解小型、中型和大型代谢网络模型的动态特性。