Abstract
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.
Highlights
Plant pathogens have evolved a variety of strategies to ensure a successful interaction with their hosts
The plant pathogen Pseudomonas syringae uses several strategies to the manipulate hormone signaling of its hosts, including production of virulence factors that alter hormone responses in and synthesis of plant hormones or hormone mimics
Synthesis of indole-3-acetic acid (IAA), a common form of the plant hormone auxin, by many plant pathogens has been implicated in virulence
Summary
Plant pathogens have evolved a variety of strategies to ensure a successful interaction with their hosts. These include the delivery of virulence proteins directly into host cells through the type III secretion system and production of plant hormones or hormone mimics. Both strategies are important for suppressing host defenses and/or modulating host physiology to promote colonization and disease development [1,2,3]. Production and secretion of coronatine modulates host jasmonic acid signaling and is important for P. syringae pathogenesis [8,9,10]. Many plant-associated microbes have the ability to synthesize indole-3-acetic acid (IAA), a common form of the phytohormone auxin, and in several cases production of IAA has been implicated in pathogen virulence [11, 12]
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