| Host-microbe interactions are of primary importance to biology, since microbes impact a wide variety of life processes. One important area of microbial influence is how pathogens like bacteria, fungi, and viruses continually drive the evolution of immune systems. Mammals and plants alike must have sophisticated recognition systems to defend themselves against microbial enemies, while at the same time, promote colonization by beneficial microbes. During my time in the Innes lab, I have been researching the molecular mechanisms underlying host-microbe interactions. Specifically, my work has focused on two main questions: 1) How do pathogens use molecular weaponry to promote virulence on susceptible hosts, and 2) How do resistant hosts detect pathogen molecules to trigger an immune response? My PhD research has provided two interesting answers to these questions. First, I demonstrated that two closely-related resistance proteins from soybean, Rpg1b and Rpg1r, use leucine-rich repeat domains to distinguish between two unrelated bacterial proteins, AvrB and AvrRpm1. My result is intriguing since Arabidopsis recognizes AvrB and AvrRpm1 with a single resistance protein, RPM1. This new knowledge provides a molecular explanation of how host resistance factors from different plant species detect specific pathogen weapons. Second, my research shows that the bacterial effector protein AvrPphB enhances the growth of Pseudomonas syringae on Arabidopsis by masking the presence of another effector that would otherwise trigger resistance. This virulence phenotype is conserved in soybean, indicating a mechanism by which AvrPphB can disrupt independently-evolved resistance machinery in two plant species. Together this work advances our understanding of the molecular and genetic factors that influence resistance and pathogenesis. |
