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Plant Cell Advance Online Publication
Published on November 17, 2006; 10.1105/tpc.105.038810

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Received October 17, 2005
Returned for revision September 20, 2006
Accepted October 26, 2006

A Constitutive Shade-Avoidance Mutant Implicates TIR-NBS-LRR Proteins in Arabidopsis Photomorphogenic Development

Ana Faigón-Soverna 1, Franklin G. Harmon 2, Leonardo Storani 3, Elizabeth Karayekov 1, Roberto J. Staneloni 4, Walter Gassmann 5, Paloma Más 6, Jorge J. Casal 1, Steve A. Kay 2, and Marcelo J. Yanovsky 1*

1 IFEVA-Facultad de Agronomía, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, 1417 Buenos Aires, Argentina
2 Department of Cell Biology and Institute for Childhood and Neglected Diseases, Scripps Research Institute, La Jolla, California 92037
3 IFEVA-Facultad de Agronomía, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, 1417 Buenos Aires, Argentina; Instituto de Investigaciones Bioquímicas, Fundación Instituto Leloir, 1405 Buenos Aires, Argentina
4 Instituto de Investigaciones Bioquímicas, Fundación Instituto Leloir, 1405 Buenos Aires, Argentina
5 Division of Plant Sciences, University of Missouri, Columbia, Missouri 65211-7310
6 Consorci Consejo Superior de Investigaciones Científicas, Institut de Recerca i Teconología Agroalimentaries, Laboratori de Genètica Molecular Vegetal, Institut de Biología Molecular de Barcelona/Jordi Girona, Barcelona 08034, Spain

* To whom correspondence should be addressed. E-mail: yanovsky{at}ifeva.edu.ar.

In plants, light signals caused by the presence of neighbors accelerate stem growth and flowering and induce a more erect position of the leaves, a developmental strategy known as shade-avoidance syndrome. In addition, mutations in the photoreceptors that mediate shade-avoidance responses enhance disease susceptibility in Arabidopsis thaliana. Here, we describe the Arabidopsis constitutive shade-avoidance1 (csa1) mutant, which shows a shade-avoidance phenotype in the absence of shade and enhanced growth of a bacterial pathogen. The csa1 mutant has a T-DNA inserted within the second exon of a Toll/Interleukin1 receptor-nucleotide binding site-leucine-rich repeat (TIR-NBS-LRR) gene, which leads to the production of a truncated mRNA. Arabidopsis plants transformed with the truncated TIR-NBS-LRR gene recapitulate the mutant phenotype, indicating that csa1 is a dominant-negative mutation that interferes with phytochrome signaling. TIR-NBS-LRR proteins have been implicated in defense responses in plants. RPS4, the closest homolog of CSA1, confers resistance to Pseudomonas syringae and complements the csa1 mutant phenotype, indicating that responses to pathogens and neighbors share core-signaling components in Arabidopsis. In Drosophila melanogaster and Caenorhabditis elegans, TIR domain proteins are implicated in both development and immunity. Thus, the dual role of the TIR domain is conserved across kingdoms.






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