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Calcium and reactive oxygen species (ROS) interact with each other and playan important role in cell signaling networks. Based on the existingmathematical models, we develop an age-dependent feedback control model tosimulate the interaction. The model consists of three subsystems: cytosoliccalcium dynamics, ROS generation from the respiratory chain in mitochondria,and mitochondrial energy metabolism. In the model, we hypothesized that ROSinduces calcium release from the yeast endoplasmic reticulum , Golgi apparatus,and vacuoles, and that ROS damages calmodulin and calcineurin by oxidizingthem. The dependence of calcium uptake by Vcx1p on ATP is incorporated into themodel. The model can approximately reproduce the log phase calcium dynamics.The simulated interaction between the cytosolic calcium and mitochondrial ROSshows that an increase in calcium results in a decrease in ROS initially (inlog phase), but the increase-decrease relation is changed to anincrease-increase relation when the cell is getting old. This could accord withthe experimental observation that calcium diminishes ROS from complexes I andIII of the respiratory chain under normal conditions, but enhances ROS when thecomplex formations are inhibited. The model predicts that the subsystem of thecalcium regulators Pmc1p, Pmr1p, and Vex1p is stable, controllable, andobservable. These structural properties of the dynamical system couldmathematically confirm that cells have evolved delicate feedback controlmechanisms to maintain their calcium homeostasis.

An Age-dependent Feedback Control Model for Calcium and Reactive Oxygen Species in Yeast Cells