Location: Emerging Pests and Pathogens Research
Project Number: 8062-21000-042-002-R
Project Type: Reimbursable Cooperative Agreement
Start Date: Feb 1, 2017
End Date: Mar 31, 2021
Objective:
The goal of this project is to elucidate the mechanisms through which IAA and possibly other forms of auxin, promote PstDC3000 growth and disease development during infection of A. thaliana. The roles that auxin plays in this plant-pathogen interaction are not well understood, as stimulation of plant cell division or growth (e.g. gall or knot formation) do not contribute to pathogenesis by PstDC3000. Rather, recent findings indicate that auxin plays at least two different roles during pathogenesis: 1) suppression of SA-mediated defenses in the host, and 2) promotion of pathogen growth via mechanism that appears to be independent of both host auxin signaling and SA-mediated defenses, possibly as a signal that directly promotes virulence in the pathogen. The proposed study, which focuses on investigating the impact of IAA on P. syringae, could change our fundamental understanding of the role of auxin during pathogenesis, and may also provide valuable new insight into the signaling molecules and events regulating pathogen gene expression during infection. Specifically, we propose to address the following objectives:
OBJECTIVE 1. Investigate the direct eddects of auxin on P. syringae strain DC3000.
OBJECTIVE 2. Investigate the contributions of auxin-regulated responses in DC3000.
OBJECTIVE 3. Investigate the biosynthetic pathways and roles of P. syringae-derived auxin during pathogenesis.
OBJECTIVE 4. Investigate the role of auxin as a virulence factor in agriculturally relevant plant-pathogen systems.
Approach:
We will use RNAseq to investigate the impact of auxin on Pseudomonas syringae biology. In addition we will use RNA-Seq to identify auxin regulated genes host plants. The data generated from this work will provide knowledge about the pathogenesis of Pseudomonas syringae and insights into mechanisms underlying disease symptom development.
