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Published on August 24, 2007; 10.1104/pp.107.106302

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Received July 26, 2007
Accepted August 14, 2007

Ethylene Is One of the Key Elements for Cell Death and Defense Response Control in the Arabidopsis Lesion Mimic Mutant Vad1

Olivier Bouchez , Carine Huard , Séverine Lorrain , Dominique Roby , and Claudine Balagué *

Laboratoire des Interactions Plantes-Microorganismes (LIPM), UMR CNRS/INRA 2594, BP 52627, 31326 Castanet-Tolosan cedex, France; Centre for Integrative Genomics, University of Lausanne, Genopode Building, CH-1015, Lausanne, Switzerland

* Corresponding author; email: Claudine.Balague{at}toulouse.inra.fr.

Although ethylene is involved in the complex cross-talk of signaling pathways regulating plant defense responses to microbial attack, its functions remain to be elucidated. The lesion mimic mutant vad1-1 (for vascular associated death), that exhibits light- conditional appearance of propagative HR-like lesions along the vascular system, is a good model for studying the role of ethylene in programmed cell death and defense. Here, we demonstrate that expression of genes associated with ethylene synthesis and signaling is enhanced in vad1-1 under lesion-promoting conditions and after plant-pathogen interaction. Analyses of the progeny from crosses between vad1-1 plants and either 35S::ERF1 transgenic plants, ein2-1, ein3-1, ein4-1, ctr1-1 or eto2-1 mutants, revealed that the vad1-1 cell death and defense phenotypes are dependent on ethylene biosynthesis and signaling. In contrast, while vad1-1- dependent increased resistance was abolished by ein2, ein3 and ein4 mutations, a positive regulation of ethylene biosynthesis (eto2-1) or ethylene responses (35S::ERF1) did not exacerbate this phenotype. In addition, VAD1 expression in response to an HR-inducing bacterial pathogen is dependent on ethylene perception and signaling. These results together with previous data, suggest that VAD1 could act as an integrative node in hormonal signaling, with ethylene acting in concert with salicylic acid, as a positive regulator of cell death propagation.




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