We report here the complete genome sequences of two Ralstonia pseu-dosolanacearum strains, isolated from the warm northeast region of Brazil. They display divergent (compatible versus incompatible) interactions with the resistant tomato line Hawaii 7996. Polymorphisms were detected in a subset of effector genes that might be associated with these contrasting phenotypes. R alstonia pseudosolanacearum is a soilborne pathogen and one of the main causal agents of the bacterial wilt (BW) disease of tomato (Solanum lycopersicum L.) and other crops (1). R. pseudosolanacearum is currently classified as a distinct species within the R. solanacearum complex, which comprises strains of phylotypes I and III (2-5). Although they are of putative exotic origin, R. pseudosolanacearum phylotype I isolates are currently disseminated in Brazil (north, northeast, and central regions) and infect mainly Solanaceae crops (tomato, peppers, eggplant, and scarlet eggplant) (6, 7). In this study, two tomato-infecting R. pseudosolanacearum strains from the warm Brazilian northeast region were sequenced in order to analyze candidate genes associated with their divergent (compatible versus incompatible) interactions with the tomato line Hawaii 7996, which is the main breeding source of BW resistance in this vegetable crop (8, 9). Strain RS 476 (sequevar I-18 from Maranhão state) is characterized by its ability to induce severe BW symptoms on Hawaii 7996 (60% incidence), whereas strain CRMRs218 (also sequevar I-18 from Pernambuco state) is able to induce severe BW symptoms in a wide range of tomato cultivars, but it is avirulent to Hawaii 7996.

Quantitative trait loci (QTL) for resistance to phytophthora root rot caused by Phytophthora capsici were investigated using two Korean P. capsici isolates and 126 F 8 recombinant inbred lines derived from a cross of Capsicum annuum line YCM334 (resistant parent) and local cv. Tean (susceptible parent). The experimental design was a split plot with two replications. Highly significant effects of pathogen isolate, plant genotype, and genotype · isolate were detected. QTL mapping was performed using a genetic linkage map covering 1486AE6 cM of the pepper genome, and consisted of 249 markers including 136 AFLPs (Amplified Fragment Length Polymorphisms), 112 SSRs (Simple Sequence Repeats) and one CAPS (Cleaved Amplified Polymorphic Sequence). Fifteen QTLs were detected on chromosomes 5 (P5), 10 (P10), 11 (P11), Pb and Pc using two data processing methods: percentage of wilted plants (PWP) and relative area under the disease progress curves (RAUD-PC). The phenotypic variation explained by each QTL (R 2 ) ranged from 6AE0% to 48AE2%. Seven QTLs were common to resistance for the two isolates on chromosome 5 (P5); six were isolate-specific for isolate 09-051 on chromosomes 10 (P10) and Pc, and two for isolate 07-127 on chromosomes 11 (P11) and Pb. The QTLs in common with the major effect on the resistance for two isolates explained 20AE0-48AE2% of phenotypic variation. The isolate-specific QTLs explained 6AE0-17AE4% of phenotypic variation. The result confirms a gene-for-gene relationship between C. annuum and P. capsici for root rot resistance.