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Published on December 31, 2008; 10.1104/pp.108.131805

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Received October 28, 2008
Accepted December 25, 2008

An integrated genomics approach to define niche establishment by Rhodococcus fascians

Stephen Depuydt , Sandra Trenkamp , Alisdair R. Fernie , Samira Elftieh , Jean-Pierre Renou , Marnik Vuylsteke , Marcelle Holsters *, and Danny Vereecke

Department of Plant Systems Biology, Flanders Institute for Biotechnology, 9052 Gent, Belgium; Department of Molecular Genetics, Ghent University, 9052 Gent, Belgium; Max-Planck Institute of Molecular Plant Physiology, University of Potsdam, 14476 Potsdam-Golm, Germany; Unite Mixte de Recherche en Genomique Vegetale, Institut National de la Recherche Agronomique, F-91057, Evry, France (S.E., J.-P. R.)

* Corresponding author; email: marcelle.holsters{at}psb.ugent.be.

Rhodococcus fascians is a Gram-positive phytopathogen that induces shooty hyperplasia on its host through the secretion of cytokinins. Global transcriptomics using microarrays combined with profiling of primary metabolites on infected Arabidopsis thaliana plants revealed that this Actinomycete modulated pathways to convert its host into a niche. The transcript data demonstrated that R. fascians leaves a very characteristic mark on Arabidopsis with an outspoken cytokinin response illustrated by the activation of cytokinin perception, signal transduction, and homeostasis. The microarray data further suggested active suppression of an oxidative burst during the R. fascians pathology and comparison with publicly available transcript datasets implied a central role for auxin in the prevention of plant defense activation. Gene ontology categorization of the differentially expressed genes hinted at a significant impact of infection on the primary metabolism of the host, which was confirmed by subsequent metabolite profiling. The much higher levels of sugars and amino acids in infected plants are presumably accessed by the bacteria as carbon and nitrogen sources to support epiphytic and endophytic colonization. Hexoses, accumulating from a significantly increased invertase activity, assumingly inhibited expression of photosynthesis genes and photosynthetic activity in infected leaves. Altogether these changes are indicative of sink development in symptomatic tissues. The metabolomics data furthermore point to the possible occurrence of secondary signaling during the interaction that might contribute to symptom development. The data are placed in the context of regulation of bacterial virulence gene expression, suppression of defense, infection phenotype, and niche establishment.






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