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

Abstract

<div><p>The bacterial pathogen <i>Pseudomonas syringae</i> modulates plant hormone signaling to promote infection and disease development. <i>P</i>. <i>syringae</i> uses several strategies to manipulate auxin physiology in <i>Arabidopsis thaliana</i> 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 <i>P</i>. <i>syringae</i> pathogenesis is not well understood. Here we demonstrate that <i>P</i>. <i>syringae</i> 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 <i>aldA</i> and a close homolog, <i>aldB</i>, lead to reduced IAA production in culture and reduced virulence on <i>A</i>. <i>thaliana</i>. 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 <i>A</i>. <i>thaliana</i>. Thus, auxin is a DC3000 virulence factor that promotes pathogenicity by suppressing host defenses.</p></div

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