Transcriptional and functional study of Arabidopsis defence response against Pseudomanas syringae.

University of Minnesota Ph.D. dissertation. January 2009. Major: Plant biological sciences. Advisor: Dr. Jane Glazebrook. 1 computer file (PDF); vii, 166 pages, appendices 1-3. Ill. (some col.)Using a reverse genetic approach, we investigated genes that are potentially important for disease resistance against the bacterial pathogen of Arabidopsis thaliana: Pseudomonas syringae. Genes that were induced at least two-fold after infection by Pseudomonas syringae pv. maculicola ES4326 were chosen as candidates for our study. Arabidopsis T-DNA mutants were ordered and assayed for bacterial growth. Mutants that consistently supported more bacterial growth than wild type controls were selected for further analysis. We also monitored expression profiles of wild-type plants and mutants with defects in key components of the defense signaling network using a microarray. The data were used to model the Arabidopsis defense network 24 hours after infection by Pseudomonas syringae pv. maculicola strain Psm ES4326. From the identified novel genes that are likely important for plant defense, I chose two members from the Arabidopsis CBP60 family, CBP60g and CBP60h, for functional analyses. Mutants of CBP60g and CBP60h are more susceptible to bacterial infection than wild type. They accumulated less SA in response to MAMP (Microbe Associated Molecular Pattern) and/or pathogen inoculations. CBP60g binds to calmodulin and the calmodulin binding is important to its function in disease resistance and SA signaling. In contrast, CBP60h does not bind calmodulin and seems to function independently of calcium signaling. A cbp60g and cbp60h double mutant is highly susceptible to Pseudomonas syringae infection; it is more susceptible than sid2 and comparable to pad4. It is likely that CBP60g and CBP60h share partially redundant and crucial functions in defense signaling. The cbp60g and cbp60h double mutant was also found to affect both SA-dependent and independent signaling pathway