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How Does Plant Immunity Restrict Bacterial virulence?
Brian Kvitko: University of Georgia; Amelia Lovelace: University of Georgia
<div>Plants present cohorts of pattern recognition receptors that are able to detect<br /="/"> “non-self” microbe-associated molecular patterns (MAMPs) such as bacterial flagellin. In <em>Arabidopsis</em><br /="/"> <em>thaliana</em> the bacterial flagellin epitope flg22 is a potent elicitor of the Pattern-Triggered-Immunity (PTI)<br /="/"> response. The introduction of the pathogen <em>Pseudomonas syringae</em> pv.<i> </i><em>tomato</em> DC3000 (Pto) into<br /="/"> PTI-activated leaves results in non-virulent stasis during which Pto fails to deliver<br /="/"> type III secretion system effectors (T3Es), does not multiply, and fails to cause symptoms. The molecular mechanisms by which PTI-associated immune outputs restrict bacterial virulence are not well understood. To gain a clearer picture of the conditions Pto experiences during PTI, we conducted an <i>in situ</i> time-course transcriptomics analysis. Exposure to PTI resulted in reduced expression of multiple virulence factors. Conversely, immune exposure was associated with the increased relative expression of motility genes and specific nutrient uptake systems. We hypothesize that nutritional restriction may represent a key mechanism of PTI. In addition, we have found that co-infiltration of Pto with 1% tryptone was sufficient to partially alleviate non-virulent stasis even in leaves with fully established PTI. Co-infiltration with tryptone was observed to restore T3E translocation in PTI induced tissue by both HR assays and using the Cya adenylate cyclase T3E translocation assay. Activity-guided fractionation linked the T3E translocation restoration activity to a small peptide. These observations are important clues towards a mechanistic understanding of the highly effective innate immune defenses of plants.</div>

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