Poster
Barbara N. Kunkel, PhD (she/her/hers)
Professor
Washington University in St. Louis
St Louis, Missouri, United States
Chia-Yun Lee
Graduate Student
Washington University in St. Louis
St. Louis, Missouri, United States
Maya Irvine
Undergraduate Student
Washington University in St. Louis
St. Louis, Missouri, United States
The plant hormone auxin plays a role in many plant-microbe interactions, including promoting pathogen growth and disease symptom development in plants infected by the foliar pathogen Pseudomonas syringae. The auxin Indole-3-acetic acid (IAA) promotes virulence of P. syringae strain PtoDC3000 on Arabidopsis and tomato, either when applied exogenously or when endogenous IAA levels are elevated. IAA promotes PtoDC3000 pathogenesis via two mechanisms: 1) suppression of salicylic acid-mediated host defenses and 2) as a microbial signal that regulates bacterial gene expression. We are investigating the mechanisms PtoDC3000 uses to sense and respond to IAA and have identified pmeR, which encodes a TetR-like transcriptional repressor, to be an important regulator of IAA-responsive gene expression. Using qRT-PCR and transcriptional reporters, we show that pmeR is induced by IAA and regulates expression of itself, as well as several other IAA-responsive genes. Plant infection assays show disruption of pmeR results in reduced bacterial growth in Arabidopsis, suggesting that the ability to sense IAA is important for virulence. While PmeR de-represses transcription of pmeR upon IAA treatment, it does not appear to directly bind IAA. Rather, our studies suggest that the auxin conjugate IAA-Lysine is a ligand for PmeR. These and other findings to be reported here demonstrate that IAA modulates bacterial gene expression and virulence through a complex signaling network.