Modification of host hormone biology is a common strategy used by plant pathogens to promote disease. For example, the bacterial pathogen strain Pseudomonas syringae DC3000 (PtoDC3000) produces the plant hormone auxin (indole-3-acetic acid [IAA]) to promote PtoDC3000 growth in plant tissue. Previous studies suggest that auxin may promote PtoDC3000 pathogenesis through multiple mechanisms, including both suppression of salicylic acid (SA)-mediated host defenses and via an unknown mechanism that appears to be independent of SA. To test if host auxin signaling is important during pathogenesis, we took advantage of Arabidopsis thaliana lines impaired in either auxin signaling or perception. We found that disruption of auxin signaling in plants expressing an inducible dominant axr2-1 mutation resulted in decreased bacterial growth and that this phenotype was suppressed by introducing the sid2-2 mutation, which impairs SA synthesis. Thus, host auxin signaling is required for normal susceptibility to PtoDC3000 and is involved in suppressing SA-mediated defenses. Unexpectedly, tir1 afb1 afb4 afb5 quadruple-mutant plants lacking four of the six known auxin coreceptors that exhibit decreased auxin perception, supported increased levels of bacterial growth. This mutant exhibited elevated IAA levels and reduced SA-mediated defenses, providing additional evidence that auxin promotes disease by suppressing host defense. We also investigated the hypothesis that IAA promotes PtoDC3000 virulence through a direct effect on the pathogen and found that IAA modulates expression of virulence genes, both in culture and in planta. Thus, in addition to suppressing host defenses, IAA acts as a microbial signaling molecule that regulates bacterial virulence gene expression.

宿主激素生物学的修饰是植物病原体促进疾病的常用策略。例如，细菌病原体丁香假单胞菌DC3000（PtoDC3000）产生植物激素生长素（吲哚-3-乙酸[IAA]）以促进PtoDC3000在植物组织中的生长。先前的研究表明，生长素可能通过多种机制促进PtoDC3000的发病机理，包括抑制水杨酸（SA）介导的宿主防御以及通过一个似乎独立于SA的未知机制。为了测试宿主生长素信号传导在发病机理中是否重要，我们利用了在生长素信号传导或知觉上受损的拟南芥品系。我们发现破坏植物生长素信号表达的诱导型显性axr2-1突变导致细菌生长减少，并且通过引入sid2-2突变抑制了该表型，这削弱了SA的合成。因此，宿主生长素信号传导是PtoDC3000正常易感性所必需的，并且参与抑制SA介导的防御。没想到，tir1 afb1 afb4 afb5缺少六种已知的生长素共受体的植物中的四种突变植物，这些植物的生长素感知能力下降，这支持增加细菌的生长水平。该突变体表现出升高的IAA水平和减少的SA介导的防御，提供了其他生长素通过抑制宿主防御而促进疾病的证据。我们还研究了IAA通过对病原体的直接影响来促进PtoDC3000毒力的假说，并发现IAA可以在培养物中和植物中调节毒力基因的表达。因此，除了抑制宿主防御外，IAA还充当调节细菌毒力基因表达的微生物信号分子。