P-173 - How local microbiota-immunity-pathogen interactions determine plant infection outcome

Crop pathogens significantly reduce agricultural production. Early interactions between the pathogen and its environment in the host determine whether the pathogen can establish and cause disease. However, how the complex spatiotemporal dynamics of plant-microbiota-pathogen interactions affect disease outcomes remains unclear. Here, we developed a spatially explicit individual-based model to explore the conditions leading to pathogen establishment or exclusion. Computational simulations of plant infection by one pathogen and one commensal predicted that plant and microbial traits, spatial arrangement, and high commensal abundance restrict pathogen colonization. While we hypothesized that immunosuppression by the pathogen could also promote commensal growth and favor co-existence in the plant tissue, we observed competitive exclusion due to spatial constraints and bottlenecks between apoplastic cavities. Both stochastic and deterministic effects occurred, sometimes leading to strong immune activation by the commensal and pathogen suppression, and sometimes leading to pathogen domination and tissue colonization. Additionally, we found that phenotypic heterogeneity for type III secretion system expression in the pathogen population improves infection success by balancing immunosuppression and fast growth. This research helps elucidate pathogen ecology in their natural context and will guide microbiome engineering efforts.