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Plant and Cell Physiology Advance Access originally published online on November 2, 2007
Plant and Cell Physiology 2007 48(12):1775-1789; doi:10.1093/pcp/pcm151
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© The Author 2007. Published by Oxford University Press on behalf of Japanese Society of Plant Physiologists. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

The fou2 Gain-of-Function Allele and the Wild-Type Allele of Two Pore Channel 1 Contribute to Different Extents or by Different Mechanisms to Defense Gene Expression in Arabidopsis

Gustavo Bonaventure1,2,*, Aurélie Gfeller1, Víctor M. Rodríguez1, Florence Armand1 and Edward E. Farmer1,*

1Gene Expression Laboratory, Plant Molecular Biology, University of Lausanne, CH-1015 Lausanne, Switzerland

*Corresponding authors: Edward E. Farmer, E-mail, Edward.Farmer{at}unil.ch; Fax, +41-21-692-4195; Gustavo Bonaventure, E-mail, gbonaventure{at}ice.mpg.de; Fax, +49-3641-57-1102.


  Abstract

The fatty acid oxygenation up-regulated 2 (fou2) mutant in Arabidopsis thaliana creates a gain-of-function allele in a non-selective cation channel encoded by the Two Pore Channel 1 (TPC1) gene. This mutant genetically implicates cation fluxes in the control of the positive feedback loop whereby jasmonic acid (JA) stimulates its own synthesis. In this study we observed extensive transcriptome reprogramming in healthy fou2 leaves closely resembling that induced by treatment with methyl jasmonate, biotic stresses and the potassium starvation response. Proteomic analysis of fou2 leaves identified increased levels of seven biotic stress- and JA-inducible proteins. In agreement with these analyses, epistasis studies performed by crossing fou2 with aos indicated that elevated levels of JA in fou2 are the major determinant of the mutant phenotype. In addition, generation of fou2 aba1-5, fou2 etr1-1 and fou2 npr1-1 double mutants showed that the fou2 phenotype was only weakly affected by ABA levels and unaffected by mutations in NPR1 and ETR1. The results now suggest possible mechanisms whereby fou2 could induce JA synthesis/signaling early in the wound response. In contrast to fou2, transcriptome analysis of a loss-of-function allele of TPC1, tpc1-2, revealed no differential expression of JA biosynthesis genes in resting leaves. However, the analysis disclosed reduced mRNA levels of the pathogenesis-related genes PDF1.2a and THI2.1 in healthy and diseased tpc1-2 leaves. The results suggest that wild-type TPC1 contributes to their expression by mechanisms somewhat different from those affecting their expression in fou2.

Keywords: Cation Flux - Jasmonic acid - 13-Lipoxygenase - Oxylipin - TPC1

Abbreviations: AOS, allene oxide synthase; bHLH, basic helix–loop–helix; CAPS, cleaved amplified polymorphic sequences; 2-DE, two-dimensional electrophoresis; DTT, dithiothreitol; ET, ethylene; fou2, fatty acid oxygenation up-regulated 2; GO, gene ontology; IEF, isoelectric focusing; JA, jasmonic acid; LOX, lipoxygenase; MALDI-TOF MS, matrix-assisted laser desorption/ionization time-of-flight mass spectrometry; MeJA, methyl jasmonate; PME, pectin methylesterase; qPCR, quantitative PCR; SA, salicylic acid; TPC1, Two Pore Channel 1; WT, wild type

2Present address: Department of Molecular Ecology, Max Planck Institute for Chemical Ecology, Hans Knöll Str. 8, Jena, D-07745, Germany.

(Received August 3, 2007; Accepted October 29, 2007)
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