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A constitutive shade-avoidance mutant implicates TIR-NBS-LRR proteins in Arabidopsis photomorphogenic development

AuthorsFaigón Soverna, Ana; Harmon, Franklin G.; Storani, Leonardo; Karayekov, Elizabeth; Staneloni, Roberto J.; Gassmann, Walter; Más, Paloma CSIC ORCID; Casal, Jorge J.; Kay, Steve A.; Yanovsky, Marcelo J.
Issue Date17-Nov-2006
PublisherAmerican Society of Plant Physiologists
CitationPlant Cell 18(11): 2919-2928 (2006)
AbstractIn 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.
Description11 pages, 10 figures.-- PMID: 17114357 [PubMed].-- PMCID: PMC1693933.-- Supplementary information available at: http://www.plantcell.org/cgi/content/full/tpc.105.038810/DC1
Publisher version (URL)http://dx.doi.org/10.1105/tpc.105.038810
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