Pseudomonas syringae DC3000-derived auxin contributes to Virulence on Arabidopsis
B. KUNKEL (1), S. McClerklin (1), S. Lee (1), R. Nwumeh (1) (1) Washington University in St. Louis, U.S.A.

The bacterial pathogen Pseudomonas syringae manipulates plant hormone signaling to promote infection and disease development. P. syringae utilizes several strategies to manipulate auxin physiology in Arabidopsis thaliana to promote pathogenesis, including synthesis of indole-3-acetic acid (IAA), the predominant form of auxin in plants, and production of virulence factors that alter auxin responses in the host. However, the role of pathogen-derived auxin in P. syringae pathogenesis is not well understood. Here we demonstrate that P. syringae strain DC3000 produces IAA via a previously uncharacterized pathway and identified an indole-3-acetaldehyde dehydrogenase, AldA, that functions in IAA biosynthesis by catalyzing the NAD-dependent formation of IAA from indole-3-acetaldehyde (IAAld). Biochemical analysis and solving of the 1.9 Å resolution x-ray crystal structure reveal key features of AldA for IAA synthesis. Disruption of aldA and a close homologue lead to reduced IAA production in culture and reduced virulence on A. thaliana. We used these mutants to explore the mechanism by which pathogen derived auxin contributes to virulence and showed that auxin produced by DC3000 suppresses salicylic acid (SA)-mediated defenses in A. thaliana. Thus, auxin can be added to the list of P. syringae strain DC3000 virulence factors

Abstract Number: P9-273
Session Type: Poster