Published Tables and Figures

Table 1. Model Variables

Table 2. Functional Forms

Table 3. Values for Parameters

All the pdf files are at original size as printed in the paper. The tiff and jpeg files are enlarged versions

Figure 1. tiff jpeg pdf Signaling circuitry governing progression of the Arabidopsis hypersensitive response to avirulent Pseudomonas syringae bacteria. Thin lines culminating in arrowheads represent metabolic transformations or sequential signaling events. Dotted lines were used to indicate pathways thought to be comparatively minor in wild type Arabidopsis. Thick lines were used for regulatory circuitry. Lines terminating in a dash-head indicate negative regulation. Mutant blocks were indicated by slashes next to the name of the mutant. Abbreviations are as follows: avr • R = functional form of complex genetically specified by an avr gene and its cognate R gene; TF = lumped term for triggering factor(s) that function downstream of molecular recognition to trigger PCD; PCD = programmed cell death; SOD = apoplastic superoxide dismutase activity; SA = total salicylic acid; CM = chorismate; Alt = hypothetical precursor in alternative SA biosynthetic pathway (likely phenylalanine).

Figure 2. tiff jpeg pdf Modeling strategy, showing dynamic interplay of computational and experimental approaches.

Figure 3. tiff jpeg pdf Model equations. For all i and j, v_ij represent fluxes, K_ij represent equilibrium constants, k_ij represent kinetic rate constants, c_ij represent proportionality constants and t_ij represent values for time delays in units of hours. The variables are normalized to basal levels and the parameters are scaled relative to basal.

Figure 4. pdf Time evolution of major signaling components following infection with bacteria carrying avrB. Simulation of wild type plants (circles) used parameter values given in Table 2. Simulation of npr1 mutant plants (triangles) and ndr1 mutant plants (squares) had the parameters NPR1 or NDR1, respectively, set to zero. A-D, Equations used for simulations were those in Figure 3. E, An additional Michaelis-Menten type term was included to incorporate postulated direct negative autoregulation of SA biosynthesis. The inability of this plot to match experimental data was taken as evidence that this feedback loop doesn’t exist, at least under the conditions simulated. F, The expression for SA-dependent, NPR1-dependent negative regulation of PCD was made to affect PCD resulting from high level accumulation of superoxide late in HR as well as PCD resulting directly from TF action. The inability of this plot to match experimental data was taken as evidence that this negative regulation affects only the latter.

Figure 5. pdf Time evolution of major signaling components following infection with bacteria carrying avrRpt2. Simulations performed and symbols chosen as in Figure 4.

Figure 6. tiff jpeg pdf Changes in system dynamics due to variations in basal flux of salicylic acid production from chorismate. The value for v₂₁ was varied ten-fold in either direction from the value listed in Table 2. A, Response to bacteria carrying avrB. B, Response to bacteria carrying avrRpt2.

Figure 7. tiff jpeg pdf Changes in system dynamics due to variations in salicylic acid degradation. The value for the rate constant for first-order decay of SA (k₂₁) was varied over a thirty-fold range (ten-fold down and three-fold up from the value listed in Table 2). Higher values of k₂₁ were not physically realistic in that if degradation exceeded production, no SA could ever accumulate. A-C, Response to bacteria carrying avrB. D-F, Response to bacteria carrying avrRpt2.

Figure 8. tiff jpeg pdf Changes in system dynamics due to variations in efficacy of superoxide-dependent, NDR1-dependent upregulation of SA biosynthesis. The value for c₂₁ was varied ten-fold in either direction from the value listed in Table 2.

Figure 9. tiff jpeg pdf Changes in system dynamics due to variations in the maximal rate of PCD. The value taken for the maximal flux of cells undergoing PCD per unit time in the presence of maximal levels of triggering factor(s) and without consideration of negative regulation of PCD or direct contributions to PCD from high superoxide levels (v₁₁) was varied ten-fold in either direction from the value listed in Table 2.