Abstract

Crosses were made between tomato (Lycopersicon esculentum Mill.) inbreds susceptible to races T2 and T3 of bacterial spot (Xanthomonas vesicatoria and Xanthomonas campestris pv. vesicatoria, respectively) and accession PI 114490 with resistance to races T1, T2, and T3. Resistance to race T2 was analyzed using the parents, F1, and F2 generations from one of the crosses. The F1 was intermediate between the parents for disease severity suggesting additive gene action. The segregation of F2 progeny fit a two-locus model (χ2 = 0.96, P = 0.9-0.5) where four resistance alleles are required for a high resistance level, two or three resistance alleles provide intermediate resistance, and zero or one resistance allele results in susceptibility. The narrow sense heritability of resistance to T2 strains was estimated to be 0.37 ± 0.1 based on F2 to F3 parent-offspring regression. A second cross was developed into an inbred backcross (IBC) population to facilitate multilocation replicated testing with multiple races. Segregation for T2 resistance in the inbred backcross population also suggested control was by two loci, lending support to the two-locus model hypothesized based on the F2 segregation. To determine if the same loci conferred resistance to the other races, selections for race T2 resistance were made in the F2 and F3 generations and for race T3 resistance in the F2 through F4 generations. Six T3 selections (F5), 13 T2 selections (F4's that diverged from seven F2 selections), and control lines were then evaluated for disease severity to races T1, T2, and T3 over two seasons. Linear correlations were used to estimate the efficiency of selecting for resistance to multiple races based on a disease nursery inoculated with a single race. Race T1 and race T2 disease severities were correlated (r ≥ 0.80, P< 0.001) within and between years while neither was correlated to race T3 either year. These results suggest that selecting for race T2 resistance in progeny derived from crosses to PI 114490 would be an effective strategy to obtain resistance to both race T1 and T2 in the populations tested. In contrast, selection for race T3 or T2 will be less likely to result in lines with resistance to the other race. PI 114490 had less resistance to T3 than to T2 or T1. Independent segregation of T2 and T3 resistance from the IBC population derived from PI 114490 suggests that T3 resistance is not controlled by the same genes as T2 resistance, supporting the linear correlation data.

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