Abstract

Hawaii 7981 tomato (Lycopersicon esculentum Mill.), resistant to race T3 of the bacterial spot pathogen [Xanthomonas campestris pv. vesicatoria (Doidge) Dye], was crossed to the susceptible tomato inbred, Fla. 7060, and subsequently F2 and backcross seed were obtained. These generations were planted in the field, inoculated with the race T3 pathogen and evaluated for disease severity over two summer seasons. Data were tested for goodness-of-fit to a model based on control by the incompletely dominant gene Xv3 that confers hypersensitivity. The F1 was intermediate in disease severity to the parents for both seasons. When data were combined over both seasons, the backcrosses fit the expected 1:1 ratios although each deviated from the expected ratio in one of the 2 years tested. The F2 did not fit the expected 1:2:1 ratio in either year or when data from the two years were combined due to a deficiency of resistant plants. Thirty-three F2 plants representing an array of disease severities and hypersensitivity reactions were selected in the second season and their F3 progeny were inoculated and evaluated for disease severity. Hawaii 7981 was significantly more resistant than the 12 most resistant F3 selections even though all expressed hypersensitivity. A hypersensitive F3 with intermediate field resistance was crossed to Hawaii 7981 and subsequently, F2 and backcross generations were obtained. These generations were field inoculated with the race T3 pathogen and evaluated for disease severity. Hawaii 7981 was significantly more resistant than the F3 parent as in the previous year. The data did not fit an additive-dominance model and epistatic interactions were significant. Thus, it appears that field resistance to race T3 of bacterial spot found in Hawaii 7981 is conferred quantitatively by Xv3 and other resistance genes. Breeding implications are discussed.

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