Innate immunity in Arabidopsis : molecular mechanisms of HOPA1 and AVRRS4 - specific disease resistance signaling pathways

The entire thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file; a non-technical public abstract appears in the public.pdf file.Title from PDF of title page (University of Missouri--Columbia, viewed on January 26, 2011).Thesis advisor: Dr. Walter Gassmann,Vita.Ph. D. University of Missouri--Columbia 2009.Plants have evolved several layers of predetermined defenses, collectively called the innate immune system. Because of its effectiveness effector-triggered immunity (ETI) is a highly valuable agronomic trait. However, ETI has the potential to be highly deleterious to the host and needs to be tightly controlled. To understand the molecular basis for ETI, I used genetic approaches. Using a loss of resistance screen, I cloned the hopA1-specific RPS6 (Resistance to Pseudomonas syringae 6) resistance gene. Using a gain of resistance screen, we cloned SRFR1 (Suppressor of RPS4-RLD), which reactivates avrRps4- and hopA1-triggered immunity. Based on the genetic, molecular, biochemical, and phylogenic evidence, we propose that SRFR1 functions in a transcriptional repressor complex that balances plant immunity and development. To date RPS4 and RPS6 are the only Arabidopsis TIR-NBS-LRR resistance genes for which P. syringae effectors are known. Both pathways are negatively regulated by SRFR1. Functional characterization of RPS6 and SRFR1 will provide an important piece of the ETI puzzle.Includes bibliographical reference