Abstract

Plants evolved mechanisms to counteract bacterial infection by preparing yet uninfected systemic tissues for an enhanced defense response, so-called systemic acquired resistance or priming responses. Primed leaves express a wide range of genes that enhance the defense response once an infection takes place. While hormone-driven defense signalling and defensive metabolites have been well studied, less focus has been set on the reorganization of primary metabolism in systemic leaves. Since primary metabolism plays an essential role during defense to provide energy and chemical building blocks, we investigated changes in primary metabolism at RNA and metabolite levels in systemic leaves of Arabidopsis thaliana plants that were locally infected with Pseudomonas syringae. Known defense genes were still activated 3–4 days after infection. Also primary metabolism was significantly altered. Nitrogen (N)-metabolism and content of amino acids and other N-containing metabolites were significantly reduced, whereas the organic acids fumarate and malate were strongly increased. We suggest that reduction of N-metabolites in systemic leaves primes defense against bacterial infection by reducing the nutritional value of systemic tissue. Increased organic acids serve as quickly available metabolic resources of energy and carbon-building blocks for the production of defense metabolites during subsequent secondary infections.

Highlights

  • During long-term co-evolution with pathogenic bacteria, plants gained the ability to prepare yet non-infected tissue for enhanced defense responses once bacteria attacked locally other parts of the plant[1,2]

  • These results indicated medium-term highly significant re-organization of primary metabolism in systemic leaves that was associated with anti-bacterial plant defense responses

  • Our results show that systemic alterations of primary metabolism are induced by bacteria infection

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Summary

Introduction

During long-term co-evolution with pathogenic bacteria, plants gained the ability to prepare yet non-infected (systemic) tissue for enhanced (primed) defense responses once bacteria attacked locally other parts of the plant[1,2] This mechanism is known as systemic acquired resistance (SAR). SAR is induced after the plant either recognized certain pathogen-associated molecular patterns (PAMPs), such as flagellin and lipopolysaccharides for PAMP-triggerd immunity (PTI), or effector proteins that are introduced into host cells by the pathogen’s Type III secretion system to suppress innate immunity for effector-triggered immunity (ETI)[3,4,5] Both PTI and ETI induce partially overlapping defense responses in infected leaves of Arabidopsis thaliana[6,7]. We discuss how alterations of tricarboxylic acid (TCA)-cycle, amino acid and sugar metabolism may serve as integrated mechanisms of primed plant defense responses

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