The network architecture of plant-pathogen interactions

Plants must contend with diverse pathogens to grow and propagate, with major implications for biodiversity, agriculture, and food security. Many pathogens use virulence molecules called effectors to modify or disable important host proteins. Plants lack an organism-wide adaptive immune system, so they are unable to maintain a repertoire of antibodies recognizing individual effectors. Instead, each plant cell maintains a smaller set of resistance genes (“R genes”) which guard the host proteins. Recent experiments suggest that each effector and each R protein interacts with many different host proteins in a complex 3-layer network. How does the structure of this network govern immune activation? We propose a simple model to study how networks of interacting molecules can be used to build an immune sensor. We show that sharp immune activation emerges from even the simplest models and that redundant R genes can act to suppress the response rather than enhancing it. We then use our model to analyze the empirical interactions between A. thaliana and P. syringae, providing an opportunity to connect molecular networks with evolutionary outcomes.