Copper is an ideal biological redox cofactor because it accepts and donates electrons with relative ease. However, free copper can interfere with other important cellular redox reactions. This means that bacteria must maintain tight control of cellular copper levels, and that copper overload is a significant immunological mechanism of cytotoxicity. In collaboration with the Argüello group at Worcester Polytechnic Institute, we obtained data measuring copper levels across the periplasmic and cytoplasmic compartments of P. aeruginosa. Using this data, we modeled copper homeostasis in P. aeruginosa as a system of chemical reactions transferring copper between protein pools according to mass action kinetics. Mathematically, this is a series of ordinary differential equations describing the fluxes between different copper pools. We used the biochemical modeling software COPASI to simulate and estimate parameters for the model. During the modeling process we determined that knowledge of the protein levels is required to accurately estimate the model parameters. Additionally, it seems necessary to invoke regulation of periplasmic cuproproteins to fit a model to the data. These results will help our collaborators design experiments that produce the most crucial information for developing a more detailed model of the copper homeostasis system in P. aeruginosa.

Mathematical model for copper homeostasis in Pseudomonas aeruginosa

253rd National Meeting (2017)

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