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Systemic Resistance in Arabidopsis Induced by Biocontrol Bacteria Is Independent of Salicylic Acid Accumulation and Pathogenesis-Related Gene Expression

Corné M. J. Pieterse, Saskia C. M. van Wees, Ellis Hoffland, Johan A. van Pelt and Leendert C. van Loon
The Plant Cell
Vol. 8, No. 8 (Aug., 1996), pp. 1225-1237
DOI: 10.2307/3870297
Stable URL: http://www.jstor.org/stable/3870297
Page Count: 13
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Systemic Resistance in Arabidopsis Induced by Biocontrol Bacteria Is Independent of Salicylic Acid Accumulation and Pathogenesis-Related Gene Expression
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Abstract

Systemic acquired resistance is a pathogen-inducible defense mechanism in plants. The resistant state is dependent on endogenous accumulation of salicylic acid (SA) and is characterized by the activation of genes encoding pathogenesis-related (PR) proteins. Recently, selected nonpathogenic, root-colonizing biocontrol bacteria have been shown to trigger a systemic resistance response as well. To study the molecular basis underlying this type of systemic resistance, we developed an Arabidopsis-based model system using Fusarium oxysporum f sp raphani and Pseudomonas syringae pv tomato as challenging pathogens. Colonization of the rhizosphere by the biological control strain WCS417r of P. fluorescens resulted in a plant-mediated resistance response that significantly reduced symptoms elicited by both challenging pathogens. Moreover, growth of P. syringae in infected leaves was strongly inhibited in P. fluorescens WCS417r-treated plants. Transgenic Arabidopsis NahG plants, unable to accumulate SA, and wild-type plants were equally responsive to P. fluorescens WCS417r-mediated induction of resistance. Furthermore, P. fluorescens WCS417r-mediated systemic resistance did not coincide with the accumulation of PR mRNAs before challenge inoculation. These results indicate that P. fluorescens WCS417r induces a pathway different from the one that controls classic systemic acquired resistance and that this pathway leads to a form of systemic resistance independent of SA accumulation and PR gene expression.

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