A Study On The Mechanisms Of Bacterial Virulence And Arabidopsis Resistance

During the complex interaction of plant and pathogen, a plant can perceive invasion of pathogen and activate various defense responses, while pathogen employs different mechanisms to overcome host defense responses. My research is focused on the molecular mechanisms of bacterial virulence and plant resistance and uses the Arabidopsis-pseudomonas syringae as a model system.Pseudomonas syringae type three secretion system is a powerful apparatus to secret effector proteins into the plant cell, and it is also the most important weapon for bacterial virulence. Little is known about the biochemical function of these effector proteins and their direct host targets. We focus on an effector protein of Pseudomonas syringae DC3000, HopAI1, to investigate the virulence mechanism of Pseudomonas syringae. Here we show that HopAI1 can interact with MPK3 and MPK6 in vitro and in vivo,indicating that they are immediate virulence targets of HopAI1 in the host. HopAI1 dephosphorylates MPK3 and MPK6, consequently suppressing MAPK (Mitogen-activated protein kinase) kinase activity and plant immune responses. Further study shows that HopAI1 dephosphorylates MPK3 and MPK6 through a unique phosphothreonine lyase activity, uncovering a novel mechanism by which the bacterium overcomes host immune responses. Our study also shows that MAPK acts upstream of AtrbohD. Upon pathogen invasion, plants activate MAPKs. MAPK activation then activate the AtrbohD-dependent oxidative burst and expression of genes which are two independent down-stream defenses responses. Pathogen resistance in plant involves multiple layers of defense responses. Contribution of different defense responses to resistance and interaction between which is complex. PAMP-triggered immunity and effector-triggered immunity are two major components of plant resistance. Through analyses of several Arabidopsis-pseudomonas syringae interactions, we found that PAMP-triggered immunity and effector-triggered immunity act synergistically to contribute to nonhost resistance. We also found that effector-triggered immunity is a major source of"basal resistance"in a compatible interaction.