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Resistance

Quantitatively Assessed Resistance to Bacterial Leaf Spot in Pepper That is Simply Inherited. A. M. Hibberd, Former graduate assistant, Vegetable Crops Department, University of Florida, Gainesville 32611, Present address: Queensland Department of Primary Industries, Box 327, Cleveland, Queensland, Australia 4163; R. E. Stall(2), and M. J. Bassett(3). (2)Professor, Plant Pathology Department, University of Florida, Gainesville 32611; (3)Professor, Vegetable Crops Department, University of Florida, Gainesville 32611. Phytopathology 78:607-612. Accepted for publication 12 November 1987. Copyright 1988 The American Phytopathological Society. DOI: 10.1094/Phyto-78-607.

Leaves were infiltrated with cells of Xanthomonas campestris pv. vesicatoria to characterize resistance in a single plant selection of PI 163189 of Capsicum annuum. This selection (189-5) contained the Bs1 gene for hypersensitivity to race 2 of the bacterial spot pathogen and was detected by rapid necrosis after inoculation of leaves with concentrated inoculum (5 × 10⁸ cfu/ml). A second type of resistance was detected with strains of races 1 and 3 after inoculation of leaves with suspensions containing 2 × 10³ cfu/ml and was quantitatively assessed by lesion numbers and lesion diameters 2 wk after inoculation. This resistance could not be detected with the concentrated inoculum. Multiplication of strains of races 1 and 3 ceased in resistant leaves from 2 to 5 days after inoculation; and by 14 days after inoculation, bacterial populations were 10³–10⁴ times fewer than in leaves of the susceptible cultivar. Early Calwonder. In studies of the inheritance of the resistance to races 1 and 3 in populations from the cross, 189-5 X Florida VR-4 (a susceptible pepper cultivar). low numbers and small diameters of lesions were controlled by the same gene. The mean number of lesions in the F¹, F², and backcross populations varied according to the bacterial strains used for inoculation. Lesion numbers in heterozygotes were few with the weakly aggressive strain, XV 77-3A of race 3, but many with the strongly aggressive strain, XV 82-8 of race 1. The same additive gene appeared to control resistance to the strain of race 1 and concomitantly, to the strain of race 3. The resistance seems to be a slow form of hypersensitivity that is best assessed by quantitative means, but that is simply inherited.