title: Auxin promotes susceptibility to Pseudomonas syringae via a mechanism independent of suppression of salicylic acid-mediated defenses.
abstract: Auxin is a key plant growth regulator that also impacts plant-pathogen interactions. Several lines of evidence suggest that the bacterial plant pathogen Pseudomonas syringae manipulates auxin physiology in Arabidopsis thaliana to promote pathogenesis. Pseudomonas syringae strategies to alter host auxin biology include synthesis of the auxin indole-3-acetic acid (IAA) and production of virulence factors that alter auxin responses in host cells. The application of exogenous auxin enhances disease caused by P. syringae strain DC3000. This is hypothesized to result from antagonism between auxin and salicylic acid (SA), a major regulator of plant defenses, but this hypothesis has not been tested in the context of infected plants. We further investigated the role of auxin during pathogenesis by examining the interaction of auxin and SA in the context of infection in plants with elevated endogenous levels of auxin. We demonstrated that elevated IAA biosynthesis in transgenic plants overexpressing the YUCCA 1 (YUC1) auxin biosynthesis gene led to enhanced susceptibility to DC3000. Elevated IAA levels did not interfere significantly with host defenses, as effector-triggered immunity was active in YUC1-overexpressing plants, and we observed only minor effects on SA levels and SA-mediated responses. Furthermore, a plant line carrying both the YUC1-overexpression transgene and the salicylic acid induction deficient 2 (sid2) mutation, which impairs SA synthesis, exhibited additive effects of enhanced susceptibility from both elevated auxin levels and impaired SA-mediated defenses. Thus, in IAA overproducing plants, the promotion of pathogen growth occurs independently of suppression of SA-mediated defenses.
authors.affiliation: Department of Biology, Washington University, St. Louis, MO 63130, USA.
authors.forename: Andrew M
authors.initials: AM
authors.lastname: Mutka
authors.forename: Stephen
authors.initials: S
authors.lastname: Fawley
authors.forename: Tiffany
authors.initials: T
authors.lastname: Tsao
authors.forename: Barbara N
authors.initials: BN
authors.lastname: Kunkel
mesh_terms: D017360:Arabidopsis / Q000235:genetics / Q000378:metabolism / Q000382:microbiology; D029681:Arabidopsis Proteins / Q000235:genetics; D018506:Gene Expression Regulation, Plant / Q000187:drug effects; D054884:Host-Pathogen Interactions / Q000187:drug effects; D007113:Immunity, Innate / Q000187:drug effects / Q000235:genetics; D007210:Indoleacetic Acids / Q000378:metabolism / Q000494:pharmacology*; D008957:Models, Genetic; D009154:Mutation; D010105:Oxygenases / Q000235:genetics; D010935:Plant Diseases / Q000235:genetics / Q000382:microbiology*; D010937:Plant Growth Regulators / Q000378:metabolism / Q000494:pharmacology; D030821:Plants, Genetically Modified; D044224:Pseudomonas syringae / Q000472:pathogenicity / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D020156:Salicylic Acid / Q000378:metabolism / Q000494:pharmacology*; D014774:Virulence
chemical_list: D029681:Arabidopsis Proteins; D007210:Indoleacetic Acids; D010937:Plant Growth Regulators; D010105:Oxygenases; C422746:YUC protein, Arabidopsis; D020156:Salicylic Acid