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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 103104 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.