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The bacterial pathogen  Pseudomonas syringae  modulates plant hormone signaling to promote infection and disease development.  P .  syringae  uses several strategies to manipulate auxin physiology in  Arabidopsis thaliana  to promote pathogenesis, including its 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 identify a novel 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, including the molecular basis of substrate specificity. Disruption of  aldA  and a close homolog,  aldB , lead to reduced IAA production in culture and reduced virulence on  A .  thaliana . We use these mutants to explore the mechanism by which pathogen-derived auxin contributes to virulence and show that IAA produced by DC3000 suppresses salicylic acid-mediated defenses in  A .  thaliana . Thus, auxin is a DC3000 virulence factor that promotes pathogenicity by suppressing host defenses.

Indole-3-acetaldehyde dehydrogenase-dependent auxin synthesis contributes to virulence of Pseudomonas syringae strain DC3000