Understanding the molecular basis of disease susceptibility of Arabidopsis to Pseudomonas syringae pv. tomato DC3000

Plant diseases are widespread and cause devastating crop losses each year. However, little is known about the molecular mechanisms of disease susceptibility to virulent pathogens. Knowledge of disease progression could be vital to designing improved methods for disease control. Pseudomonas syringae pv. tomato strain DC3000 (Pst DC3000), an important model for studying plant-pathogen interactions, causes bacterial speck on tomato and Arabidopsis thaliana. Pst DC3000 enters plants through natural openings such as stomata and wounds. It is an extracellular pathogen that must suppress or evade plant defenses and obtain nutrients from the host to be successful. Disease progression is typified by bacterial multiplication and development of water soaking followed by chlorosis and necrosis in the infected tissues. Pst DC3000 relies on the type III secretion system to deliver protein effectors across the plant cell wall into the host cell. These effectors are essential for pathogenesis as demonstrated by the inability of hrp mutants to multiply or cause disease on otherwise susceptible hosts.; To gain insight into the function of Pst DC3000 effectors in the host cell, I created transgenic Arabidopsis plants that express avrPto. I showed that transgenic expression of avrPto repressed a set of Arabidopsis genes that were also repressed during Pst DC3000 infection. In addition, avrPto plants permitted enhanced multiplication of a Pst DC3000 hrp mutant, an avirulent derivative of Pst DC3000, and P. fluorescens (a non-phytopathogenic bacterium). The increased growth of these bacteria in avrPto plants is not correlated with water-extractible nutrients in the apoplastic space, but is associated with impaired host extracellular defense and secretion. avrPto plants were unable to deposit defense-related callose in the cell wall. Furthermore, several host proteins that are present in the apoplast of wild-type plants inoculated with an avirulent pathogen were absent in avrPto plants. Based on these and other results, we postulate that one virulence function of AvrPto in Arabidopsis is to promote pathogenesis by interfering with host trafficking to the extracellular space.; In addition to determining how AvrPto operates in the plant cell, I investigated host components that are involved in disease symptom development. An Arabidopsis mutant screen uncovered a mutant that did not develop disease-associated chlorosis in response to Pst DC3000 infection. The growth and development of this mutant, noc1 ( no-c&barbelow;hlorosis1), is not different from wild-type, but the noc1 plants lose chlorophyll at a slower rate than wild-type plants during disease development. Both noc1 and wild-type plants had similar increased transcript levels of AtCIh1I (a gene in the chlorophyll degradation pathway) upon Pst DC3000 infection. The noc1 gene is located on the long arm of chromosome 4.; The information gained from this research may lead to an increased understanding of the molecular processes that occur during Pst DC3000 infection of susceptible Arabidopsis.