UC Berkeley

The research of plant –microbe interactions is a field with broad applications and strong economic importance to society, as plants are the primary producers that we rely upon for food, textiles, air quality and ornamental value. Global climate change is predicted have a dramatic impact on plant-microbe and pest interactions, and better understanding of how plants respond to pathogen threats is important. The plant hormone salicylic acid (SA) is a crucial signaling molecule in the response to infection by (hemi)biotrophic microbes, as well as other abiotic stress responses. However, our understanding of the mechanisms governing its synthesis is lacking. Pathogen challenge induces rapid and robust SA synthesis, increasing the amount of the hormone 10-fold within 48 hours. However, SA synthesis also occurs at a low rate in uninfected plants, accumulating as a storage form that can be readily converted to active SA. Herein, I detail two studies using the model dicot Arabidopsis thaliana examining the processes governing SA accumulation through metabolic manipulation of SA precursors and transporters, and show that the pre-infection levels of endogenous SA can play a role in priming plant immunity.

In chapter 2, I present evidence that chorismate mutases can influence basal SA synthesis by their competition with isochorismate synthase enzymes for the substrate chorismate. Transient overexpression of these enzymes reduced SA accumulation in planta, suggesting these enzymes redirected chorismate flux away from SA synthesis. Plants with reduced expression of chorismate mutase 1 (CM1) exhibited elevated basal SA levels, which conferred enhanced disease resistance to a virulent bacterial Pseudomonas syringae foliar pathogen. This phenotype comes without an obvious fitness cost to the plant; they don’t exhibit increased basal expression of defense genes, or a reduction in plant growth. Rather, it appears that this elevated basal SA quickens early responses to pathogens, a key moment in the infection process.

In contrast, chapter 3 details the discovery that the transcriptional repressor DEL1, previously characterized for its role as a cell cycle regulator, also mediates basal SA synthesis. Loss of DEL1 repression leads to increased expression of SA biosynthesis and transporter genes, which alters SA signaling responses and primes the plant for greater disease resistance to both bacterial and fungal pathogens. CM1 and DEL1 mutant plants represent a continuum of defense priming by endogenous SA, and illustrate new approaches for modulating increased disease resistance in plants by influencing metabolic flux of chorismate products. The discovery that DEL1 also mediates expression of an SA hub suggests that it plays a broader role in coordinating developmental and stress response cues.