Mechanisms of bacterial virulence and plant disease resistance

Many gram negative bacterial pathogens use the type III secretion system to inject proteins directly into host cells. These type III effectors often target specific host proteins to modify the cellular environment to favor the infection process. This can lead to an observable increase in the virulence of pathogens expressing specific type III effectors. During plant-pathogen interactions, these effectors can also betray the bacteria since plants have evolved resistance (R) proteins to detect the modifications induced by effectors and subsequently mount effective defense responses to thwart the infection process. Consequently, certain bacterial effectors have evolved to mask the presence of others, making the pathogen undetectable by the plants surveillance system. Therefore, by injecting a suite of proteins into the host cell, bacteria induce a complex series of molecular modifications which determine the outcome of a plant-pathogen interaction: disease or resistance.

My research focuses on understanding how type III effectors secreted by phytopathogenic bacteria manipulate host cellular metabolism to favor infection and how plants have evolved to recognize invading pathogens to mount effective defense responses. Understanding the molecular events induced by type III effectors during a host-pathogen interaction initially requires the establishment of a network map of effector interactions and characterization of how the targets are modified. This information can then be integrated in order to understand the interplay between the multiple type III effectors injected by a bacterial strain into host cells and how this series of events enhance virulence or trigger defense responses. The similarities between plant and animal innate immune systems and the common virulence mechanisms used by bacterial pathogens of plants and animals make the experimentally advantageous plant-pathogen system an ideal model to study bacterial pathogenesis of eukaryotic organisms.