Abstract
Our understanding of how, and the extent to which, phytopathogens reconfigure host metabolic pathways to enhance virulence is remarkably limited. Here we investigate the dynamics of the natural disaccharide nucleoside, 3′-O-β-D-ribofuranosyladenosine, in leaves of Arabidopsis thaliana infected with virulent Pseudomonas syringae pv. tomato strain DC3000. 3′-O-β-D-ribofuranosyladenosine is a plant derived molecule that rapidly accumulates following delivery of P. syringae type III effectors to represent a major component of the infected leaf metabolome. We report the first synthesis of 3′-O-β-D-ribofuranosyladenosine using a method involving the condensation of a small excess of 1-O-acetyl-2,3,5-three-O-benzoyl-β-ribofuranose activated with tin tetrachloride with 2′,5′-di-O-tert-butyldimethylsilyladenosine in 1,2-dichloroethane with further removal of silyl and benzoyl protecting groups. Interestingly, application of synthetic 3′-O-β-D-ribofuranosyladenosine did not affect either bacterial multiplication or infection dynamics suggesting a major reconfiguration of metabolism during pathogenesis and a heavy metabolic burden on the infected plant.
Highlights
Our understanding of the genetic basis of plant innate immunity has improved greatly over the past two decades
The rapid appearance of 3′-Oβ-D-RFA was striking as bacterial effectors are not delivered into the plant cells until ∼3 hpi after challenge and DC3000 multiplication does not occur under those conditions until ∼8 hpi (Lewis et al, 2015)
To rule out the possibility 3′-O-β-D-RFA is of bacterial origin we used a transgenic A. thaliana line conditionally expressing the P. syringae effector HopAM1 from a dexamethasone inducible promoter in Wassilewskija background (Goel et al, 2008)
Summary
Our understanding of the genetic basis of plant innate immunity has improved greatly over the past two decades. We understand the core receptors involved in the two key immunity responses, the initial MAMP (microbe associated molecular patterns) triggered immunity (MTI) and subsequent effector triggered immunity (ETI) where activity of pathogen effectors delivered into the plant cell are recognized by classical plant disease resistance proteins (Jones and Dangl, 2006). We are unravelling the basis of suppression of plant immunity, driven by pathogen effectors (primarily proteins, and small molecules), which suppress MTI and ETI to cause disease (effector triggered suppression, ETS; (Boutrot and Zipfel, 2017; Jones and Dangl, 2006)). The rapid induction of 3′-O-β-DRFA to high levels upon infection in both tomato and A. thaliana precedes reported increases in indole derivatives (Bednarek et al, 2004; Ward et al, 2010) and suggests an important role in suppression of plant immunity
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
