| My thesis work is focused on understanding the molecular mechanisms controlling programmed cell death induced by biotic and abiotic stress in plants. Cellular suicide upon pathogen infection is a highly effective strategy for restricting pathogen growth and disease spread by blocking pathogen access to water and nutrients. Prior work in the Innes laboratory identified two Arabidopsis genes involved in the control of programmed cell death upon fungal infection, EDR1 (Enhanced Disease Resistance 1) and KEG (Keep On Going). Loss-of-function mutations in EDR1 cause extensive host cell death upon infection, while missense mutations in KEG fully suppresses the uncontrolled cell death in edr1 mutants. In chapter 2 of this dissertation, I show that the EDR1 and KEG proteins co-localize to small intracellular membrane-bound vesicles called endosomes. I further demonstrate a direct interaction between these two proteins on endosomes. Chapter 3 presents my analyses of KEG's role in endomembrane transport pathways, which revealed that endosomes may function as signaling platforms to regulate defense responses and stress-induced cell death. Consistent with this model, I found that KEG is targeted for degradation by the fungal pathogen Golovinomyces cichoracearum, causal agent of powdery mildew disease on Arabidopsis, suggesting that pathogens have learned to manipulate KEG to suppress defense responses. In chapter 4, I describe the identification of a second EDR1-interacting protein named ATL1 (ARABIDOPSIS TOXICOS EN LEVADURA 1), which also localizes to endosomes. I found that overexpression of ATL1 induces cell death, while co-expression with EDR1 suppresses ATL1-induced death, indicating that both ATL1 and KEG activities are regulated by EDR1. |
