20 November 2009
Department of Biology
Department of Mathematics
Metabolic networks are typically analyzed under the assumption that they operate at steady-state. System properties such as control coefficients and robustness are studied by small perturbations of the steady-state, and the evolution of such networks is assumed to be driven by maximization or optimization of steady-state fluxes. Nothing could be farther from reality. In life, metabolic systems are subject to continuous and large fluctuations in input and demand, and the expression levels of many genes vary dramatically during the day. We will discuss our studies on the dynamics of metabolic networks, concentrating on (1) folate and glutathione metabolism, and (2) dopamine and serotonin metabolism. Our studies show that stability and robustness in metabolic networks is due to dynamically active homeostatic mechanisms, rather than passive establishment of a steady-state. Similar non-steady-state processes undoubtedly operate in genetic networks and signaling networks as well.
For more details and papers see metabolism.math.duke.edu/
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