The metabolic transition during disease following infection of Arabidopsis thaliana by Pseudomonas syringae pv. tomato

Jane L. Ward(Aberystwyth University), Silvia Forcat(Imperial College London), Manfred Beckmann(Aberystwyth University), Mark H. Bennett(Imperial College London), Sonia J. Miller(Rothamsted Research), John M. Baker(Rothamsted Research), N. Hawkins(Rothamsted Research), Cornelia P. Vermeer(Aberystwyth University), Chuan Lü(Aberystwyth University), Wanchang Lin(Aberystwyth University), William M. Truman(University of Exeter), Michael H. Beale(Rothamsted Research), John Draper(Aberystwyth University), John W. Mansfıeld(Imperial College London), Murray Grant(University of Exeter)
The Plant Journal
May 18, 2010
Cited by 202Open Access
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Abstract

The outcome of bacterial infection in plants is determined by the ability of the pathogen to successfully occupy the apoplastic space and deliver a constellation of effectors that collectively suppress basal and effector-triggered immune responses. In this study, we examined the metabolic changes associated with establishment of disease using analytical techniques that interrogated a range of chemistries. We demonstrated clear differences in the metabolome of Arabidopsis thaliana leaves infected with virulent Pseudomonas syringae within 8 h of infection. In addition to confirmation of changes in phenolic and indolic compounds, we identified rapid alterations in the abundance of amino acids and other nitrogenous compounds, specific classes of glucosinolates, disaccharides, and molecules that influence the prevalence of reactive oxygen species. Our data illustrate that, superimposed on defence suppression, pathogens reconfigure host metabolism to provide the sustenance required to support exponentially growing populations of apoplastically localized bacteria. We performed a detailed baseline study reporting the metabolic dynamics associated with bacterial infection. Moreover, we have integrated these data with the results of transcriptome profiling to distinguish metabolomic pathways that are transcriptionally activated from those that are post-transcriptionally regulated.


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