Chia-Yun Lee’s research while affiliated with Washington University in St. Louis and other places

Plant pathogenic bacteria, such as Pseudomonas syringae strain Pto DC3000, respond to host signals through complex signaling networks that regulate bacterial growth and virulence. The plant hormone indole-3-acetic acid (IAA), also known as auxin, promotes bacterial pathogenesis via multiple mechanisms, including through reprogramming bacterial transcription. However, the mechanisms that Pto DC3000 uses to sense and respond to auxin are not well understood. Here, we identify pmeR , which encodes a TetR-like family transcriptional repressor, as an important regulator of IAA-responsive gene expression in Pto DC3000. Using qRT-PCR and transcriptional reporter assays, we show that pmeR is induced by IAA and regulates a set of auxin-responsive genes, including itself as well as several genes known or proposed to be involved in virulence. Plant infection assays further show that the disruption of pmeR results in reduced bacterial growth in Arabidopsis thaliana . Notably, while PmeR de-represses transcription of pmeR upon IAA treatment, it does not appear to directly bind IAA. Rather, our biochemical results indicate that the auxin conjugate IAA-Lysine may serve as a ligand for PmeR. Our findings reveal a complex signaling network through which IAA modulates bacterial gene expression and emphasizes the role of PmeR in acclimating Pto DC3000 for growth in plant tissue. Author Summary Plant pathogenic bacteria, such as Pseudomonas syringae strain Pto DC3000, respond to host signals through complex signaling networks that regulate bacterial growth and virulence. One key signal involved in these interactions is the plant hormone indole-3-acetic acid (IAA), which has been shown to promote bacterial pathogenicity in Arabidopsis thaliana and tomato. However, the mechanisms Pto DC3000 uses to sense and respond to IAA remain poorly understood. In this study, we explored the role of the TetR-like transcriptional regulator PmeR, encoded by the pmeR gene, in regulating bacterial responses to IAA. We found that pmeR is induced by IAA and regulates the expression of several additional auxin-responsive genes. Furthermore, we showed that pmeR is required for full virulence of Pto DC3000 in A. thaliana . These results suggest that PmeR is involved in regulating IAA-induced gene expression and that the ability to respond to auxin contributes to virulence of Pto DC3000. This work sheds new light on the molecular mechanisms through which IAA regulates bacterial pathogenesis, providing important insights into plant-microbe interactions and the role of auxin in regulating bacterial behavior. Our findings offer potential directions for developing strategies to mitigate bacterial diseases in crops by targeting auxin-responsive regulatory pathways.

Several plant-associated microbes synthesize the auxinic plant growth regulator phenylacetic acid (PAA) in culture; however, the role of PAA in plant-pathogen interactions is not well understood. In this study, we investigated the role of PAA during interactions between the phytopathogenic bacterium Pseudomonas syringae strain PtoDC3000 (PtoDC3000) and the model plant host, Arabidopsis thaliana. Previous work demonstrated that indole-3-acetaldehyde dehydrogenase A (AldA) of PtoDC3000 converts indole-3-acetaldehyde (IAAld) to the auxin indole-3-acetic acid (IAA). Here, we further demonstrated the biochemical versatility of AldA by conducting substrate screening and steady-state kinetic analyses, and showed that AldA can use both IAAld and phenylacetaldehyde as substrates to produce IAA and PAA, respectively. Quantification of auxin in infected plant tissue showed that AldA-dependent synthesis of either IAA or PAA by PtoDC3000 does not contribute significantly to the increase in auxin levels in infected A. thaliana leaves. Using available arogenate dehydratase (adt) mutant lines of A. thaliana compromised for PAA synthesis, we observed that a reduction in PAA-Asp and PAA-Glu is correlated with elevated levels of IAA and increased susceptibility. These results provide evidence that PAA/IAA homeostasis in A. thaliana influences the outcome of plant-microbial interactions.

Several plant-associated microbes synthesize the auxinic plant growth regulator phenylacetic acid (PAA) in culture; however, the role of PAA in plant-pathogen interactions is not well understood. In this study, we investigate the role of PAA during interactions between the phytopathogenic bacterium Pseudomonas syringae strain Pto DC3000 ( Pto DC3000) and the model plant host, Arabidopsis thaliana . Previous work demonstrated that indole-3-acetaldehyde dehydrogenase A (AldA) of Pto DC3000 converts indole-3-acetaldehyde (IAAld) to the auxin indole-3-acetic acid (IAA). Here, we further demonstrate the biochemical versatility of AldA, as it can use both IAAld and phenylacetaldehyde as substrates to produce IAA and PAA, respectively. We also show that during infection AldA-dependent synthesis of either IAA or PAA by Pto DC3000 does not contribute significantly to the increase in auxin levels in A. thaliana leaves. Using available arogenate dehydratase ( adt ) mutant lines of A. thaliana compromised for PAA synthesis, we observed that a reduction in PAA-Asp and PAA-Glu is correlated with elevated levels of IAA and increased susceptibility. These results provide evidence that PAA/IAA homeostasis in A. thaliana influences the outcome of plant-microbial interactions.