E. Wicker, and
First, sixth, seventh, and eighth authors: CIRAD, UMR Peuplements Végétaux et Bioagresseurs en Milieu Tropicale (PVBMT), 7 Chemin de l'IRAT, 97410, Saint-Pierre Cedex, La Réunion; second and fourth authors: Institut National de la Recherche Agronomique (INRA), Centre d'Avignon, UR 1052, Unité de Génétique et Amélioration des Fruits et Légumes, Domaine St. Maurice, BP 94, 84143 Montfavet Cedex, France; third author: Department of Molecular Biology and Genetics, Izmir Institute of Technology, Urla, Izmir, 35430, Turkey; fifth author: Asian Vegetable Research Development Center–The World Vegetable Center, P.O. Box 42, Shanhua, Tainan, Taiwan 741, R.O.C.; and ninth author: INRA/CIRAD, UMR PVBMT, 7 Chemin de l'IRAT, 97410, Saint-Pierre Cedex, La Réunion.
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Accepted for publication 24 August 2010.
Bacterial wilt, caused by strains belonging to the Ralstonia solanacearum species complex, inflicts severe economic losses in many crops worldwide. Host resistance remains the most effective control strategy against this disease. However, wilt resistance is often overcome due to the considerable variation among pathogen strains. To help breeders circumvent this problem, we assembled a worldwide collection of 30 accessions of tomato, eggplant and pepper (Core-TEP), most of which are commonly used as sources of resistance to R. solanacearum or for mapping quantitative trait loci. The Core-TEP lines were challenged with a core collection of 12 pathogen strains (Core-Rs2) representing the phylogenetic diversity of R. solanacearum. We observed six interaction phenotypes, from highly susceptible to highly resistant. Intermediate phenotypes resulted from the plants' ability to tolerate latent infections (i.e., bacterial colonization of vascular elements with limited or no wilting). The Core-Rs2 strains partitioned into three pathotypes on pepper accessions, five on tomato, and six on eggplant. A “pathoprofile” concept was developed to characterize the strain clusters, which displayed six virulence patterns on the whole set of Core-TEP host accessions. Neither pathotypes nor pathoprofiles were phylotype specific. Pathoprofiles with high aggressiveness were mainly found in strains from phylotypes I, IIB, and III. One pathoprofile included a strain that overcame almost all resistance sources.
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