A genome-scale metabolic model of a pathosystem sheds light on bacterial wilt.

During plant infection, complex metabolic interactions occur between the host and the pathogen, including direct competition for resources. While pathogens exploit host-derived nutrients to sustain growth and virulence, plants attempt to restrict pathogen proliferation by limiting nutrient availability. To quantify the contribution of these trophic interactions to disease development, we developed a mathematical model of plant-pathogen metabolism. A genome-scale metabolic model of the pathogen was integrated with a genome-scale, multiorgan metabolic model of the plant and calibrated using experimental data. Model simulations were performed using a sequential flux balance analysis framework. This approach was applied to the Ralstonia pseudosolanacearum-tomato (Solanum lycopersicum) pathosystem. Quantitative fluxes of matter occurring during plant infection were predicted. The model shows that (i) plant photosynthetic capacity imposes a stronger constraint on bacterial proliferation than mineral availability; (ii) infection-induced reduction in plant transpiration first limits plant growth and subsequently restricts pathogen expansion; (iii) stem resource hijacking enhances bacterial growth but is likely limited; and (iv) pathogen-excreted putrescine is likely reutilized for the plant's needs. Together, these results provide a quantitative assessment of resource competition in plant-pathogen interactions and highlight the central role of water flow during infection by a fast-growing, xylem-colonizing bacterium.