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Isolation and Characterization of a Novel Arabidopsis thaliana Mutant Unable to Develop Wilt Symptoms After Inoculation with a Virulent Strain of Ralstonia solanacearum

March 2004 , Volume 94 , Number  3
Pages  289 - 295

Dong-Xin Feng , Laurent Deslandes , Harald Keller , Frédéric Revers , Bruno Favery , Philippe Lecomte , Judith Hirsch , Jocelyne Olivier , and Yves Marco

First, seventh, eighth, and ninth authors: Laboratoire des Interations Plantes-Microorganismes, CNRS/INRA, Chemin de Borde-Rouge, BP 27, Castanet-Tolosan, 31326, France; second author: Max-Planck-Institut für Züchtungsforschung, Abteilung Biochemie, Carl von Linné Weg 10, D-50829 Köln, Germany; third, fifth, and sixth authors: Institut National de la Recherche Agronomique, Station de Botanique et de Pathologie Végétale, BP 2078, 06606 Antibes Cedex, France; and fourth author: Virologie Végétale, IBVM-INRA Bordeaux-Aquitaine, Villenave d'Ornon, France

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Accepted for publication 4 November 2003.

To characterize host genes required for a compatible interaction, we identified a novel recessive Arabidopsis thaliana mutant, nws1 (no wilt symptoms), that failed to develop wilt symptoms in response to virulent strains of the phytopathogenic bacterium, Ralstonia solanacearum. The absence of wilting in nws1 plants was not correlated with a cell death phenotype or a constitutive expression of salicylic acid-, jasmonic acid- or ethylene-associated genes. In addition, this mutation, which conferred a symptomless phenotype in response to all the R. solanacearum strains tested, was highly specific to this pathogen, because nws1 responses to other plant pathogens, including oomycetes, nematodes, viruses, and other bacteria, were identical to those of wild-type Col-5 plants. Finally, the lack of disease development was shown to be different than RRS1-R-mediated resistance. The identification of mutants such as nws1, that are unable to develop disease, should lead to the isolation of target host factors required for pathogen growth or fitness, or of factors modified by the invading microorganism to avoid or inactivate plant defense mechanisms, and should bring a better understanding of bacterial wilt diseases.

© 2004 The American Phytopathological Society