Off-campus UNL users: To download campus access dissertations, please use the following link to log into our proxy server with your NU ID and password. When you are done browsing please remember to return to this page and log out.
Non-UNL users: Please talk to your librarian about requesting this dissertation through interlibrary loan.
Pseudomonas syringae Pathogenesis and Suppression of Plant Immunity
The Gram-negative bacterial plant pathogen Pseudomonas syringae requires a type III protein secretion system (T3SS) to cause disease. In this thesis, I describe three projects that I was involved with during my PhD studies. The first is on the T3E HopE1. This T3E uses the calcium sensor-calmodulin (CaM), as a co-factor to target the microtubule-associated protein 65 (MAP65). HopE1 interacted with MAP65 in a CaM-dependent manner, resulting in MAP65-GFP dissociation from microtubules. Additionally, Arabidopsis map65-1 mutants were immune deficient and were more susceptible to P. syringae. These suggest HopE1 effector is activated by host CaM to target MAP65, thereby inhibiting cell wall-based immunity. ^ The second is focused GRP7, a plant target of the T3E HopU1. We found that GRP7 transgenic plants were more resistant to hemi- or biotrophic pathogens and induced levels of PRs after pathogen infection. Importantly, the increased resistance of GRP7 transgenic plants was dependent on salicylic acid (SA)-mediated immunity. The interaction between GRP7 and immunity-related RNAs was inhibited by HopU1 in a manner dependent on HopU1’s ADP-RT activity. I performed RNA immunoprecipitation-sequencing experiments and found that many RNAs interacted with GRP7 including many more immunity-related. Our research reveals the broad role of GRP7 in plant immunity. ^ The third is focused on P. syringae’s ability to alter Arabidopsis histone modification. P. syringae to reduce H3K9 levels was dependent on a functional T3SS and is correlated with the suppression of immunity-related gene expression. Moreover, chromatin immunoprecipitation experiments showed that promoters of immunity-related genes had reduced H3K9ac levels in plants infected with P. syringae . Many T3Es can reduce H3K9 levels. This was likely indirect through their general ability to suppress plant immunity. Arabidopsis hda5 mutants were more resistant to P. syringae and showed increased production of callose deposition. These mutants also no longer exhibited decreased levels of H3K9ac associated with immunity-related genes upon infection with P. syringae suggesting that the reduction of H3K9ac levels in plants infected by P. syringae was due to HDA5. Therefore, HDA5 acts as a negative regulator of plant immunity and P. syringae can directly or indirectly employ it to aid in immunity suppression.^
Molecular biology|Plant pathology
Kim, Panya, "Pseudomonas syringae Pathogenesis and Suppression of Plant Immunity" (2017). ETD collection for University of Nebraska - Lincoln. AAI10643134.