Application of gene expression profiling for analyzing plant disease resistance

Plants respond to pathogen infection by inducing various defense responses regulated through a signaling network. The relationship between a resistant host plant and an avirulent pathogen is called an incompatible interaction, while that between a susceptible host plant and a virulent pathogen is called a compatible interaction. The goal of this study is to understand molecular events underlying the two interactions. A model plant-pathogen system composed of the plant host Arabidopsis thaliana and the bacterial pathogen Pseudomonas syringae was used to take advantage of their genetic and genomic tractability. During incompatible interactions, resistant plants induce defense responses through an R protein-mediated specific recognition of a corresponding pathogen Avr protein. Interactions between R and Avr often involve other proteins. A p75 protein interacts with both resistance protein RPS2 and the corresponding avirulence protein, AvrRpt2. I showed that the region of RPS2 that interacts with p75 resides in the N-terminal 326 residues. Global expression profiling was used to characterize incompatible and compatible interactions in detail and to identify novel candidate genes involved in downstream signaling events. A direct comparison of expression profiles between compatible and incompatible interactions revealed that the difference is largely quantitative and kinetic. An expression pattern transformation from an early to a late expression pattern was observed during both interactions, although the expression profiles of the compatible interactions were of low amplitude. During the compatible and incompatible interactions, a kinetic difference in pattern transformation was demonstrated, which results from the activation of gene-for-gene resistance during the incompatible interactions. Hsf4 is one of the genes whose expression is up-regulated upon pathogen infection. Hsf4 is preferentially induced during incompatible interactions. Plants with reduced Hsf4 expression showed enhanced disease resistance to a strain of virulent Pseudomonas bacteria pathogen. This suggests that induced expression of Hsf4 facilitates bacterial growth. Plants that over-express Hsf4 exhibit morphological abnormalities and reduced fertility. In addition, Hsf4 is required for heat shock induced Hsp expression. These results suggest that Hsf4 is involved in multiple cellular processes. Thus, in this thesis, I characterized incompatible interaction using both gene expression profiling and reverse genetics approaches.