Understanding the priming response in Systemic Acquired Resistance and Age-Related Resistance

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Plants possess a number of disease resistance pathways to combat microbial infections. Each year an estimated 40% of world food production is lost due to insects, weeds and disease despite resistant crop varieties and pesticide application. In view of these losses, the goal of my research team is to understand Systemic Acquired Resistance (SAR) and Age-related Resistance (ARR). Both SAR and ARR involve a priming stage in which an initial biological, chemical or developmental stimulus allows a plant to respond rapidly and effectively to subsequent pathogen infections. Understanding these priming mechanisms will provide insights for genetic and breeding strategies to allow crops to respond rapidly and effectively to disease. *** SAR is induced by an "immunizing" infection in one leaf producing SAR signals that move to uninfected leaves to prime plants to respond in a resistant manner to future infections. The outcome of SAR is similar to vaccination in mammals, however SAR is more effective as it protects plants against many different pathogens. We study a key player in SAR called DIR1. DIR1 encodes a lipid transfer protein (LTP) and in vitro it binds lipids in its hydrophobic binding cavity. We hypothesize that DIR1 binds a lipid and/or hydrophobic molecule and this complex moves to distant tissues to prime distant leaves to resist future pathogen infections. We discovered that DIR1 moves to distant tissue to initiate priming and created a number of tools to identify DIR1's binding partners. We are in position to understand how DIR1 and its binding partners are perceived in distant leaves to prepare plants to resist the next infection. This information will inform future manipulations to improve crop disease resistance.*** We also study ARR, in which a maturity-associated developmental trigger primes mature plants to respond in a highly resistant manner to normally virulent pathogens. We identified genes required for ARR including the flowering regulator SVP. In the interaction between plants and bacterial pathogens, many pathogens have evolved the ability to suppress plant defense. Our data support the hypothesis that SVP plays a role in preventing the bacterial pathogen, Pseudomonas syringae from suppressing the accumulation of anti-microbial salicylic acid (SA). By examining SA accumulation in wild type and svp mutants, combined with next generation RNA-sequencing, ChIP-qPCR, genetic suppressor screening and yeast-2-hybrid, we will discover how SVP controls ARR. Our research suggests that during ARR, plants use a novel mechanism to defend themselves by targeting and preventing the pathogen's ability to suppress defense. Understanding this novel defense mechanism will provide fundamental information enhancing our ability to manipulate this pathway to extend the highly effective ARR response to young crop plants.********