Programmed cell death (PCD) is one of the plants' defense mechanisms against invading pathogens. This highly localized cell death limits the spread of the infection and triggers whole plant antimicrobial and immune responses. Hence control over PCD can be central in determining susceptibility or resistance to disease. PCD resulting from infection of Arabidopsis thaliana plants with Pseudomonas syringae bacterial pathogens was chosen as the model system. A signaling circuitry governing progression of the Arabidopsis hypersensitive response to avirulent Pseudomonas syringae bacteria has been proposed. This circuitry hypothesis was tested by construction of a differential equations-based mathematical model.

Model-based simulations predicted time evolution of signaling components in the circuitry. The simulations studied the behavior of three different lines of Arabidopsis used in laboratory studies:  the npr1 mutant, the ndr1 mutant and wild type Arabidopsis. Two different case studies have been carried out for each of these three mutants. They are high level inoculum and low level inoculum of the Pseudomonas syringae bacteria on these mutants. In addition, response to different bacterial strains that elicited signaling with different kinetics were modeled.  The plots of the signaling components have been obtained from the simulation of the differential equations-based mathematical model run in MATLAB.  This model incorporates spatiotemporal dimensions of signaling as well as compartmentation, feedback and regulation of the processes.  Simulations of alternative circuitry hypotheses have already served to correct signaling hypotheses.  Further simulations of this nature are in progress.