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Cytology and Histology

Histopathology of Resistant and Susceptible Tomato Fruit Infected with Rhizoctonia solani. A. Bassi, Jr., Former graduate student, Department of Horticulture, Mississippi State University, Mississippi State, 39762, Present address of senior author: Department of Plant Pathology, University of Arkansas, Fayetteville, 72701; E. L. Moore(2), and W. E. Batson, Jr.(3). (2)Professor, Department of Horticulture, Mississippi State University, Mississippi State, 39762; (3)Associate professor, Department of Plant Pathology and Weed Science, Mississippi State University, Mississippi State, 39762. Phytopathology 69:556-559. Accepted for publication 13 November 1978. Copyright 1979 The American Phytopathological Society. DOI: 10.1094/Phyto-69-556.

Histopathological and anatomical differences were detected in the carpel walls of tomato fruit of PI 193407, a plant introduction reported to be resistant to soil rot caused by Rhizoctonia solani, and Campbell-28 (C-28), a susceptible cultivar. Cells of the epidermal layer, subepidermal layer, and underlying parenchyma were larger and more consistent in size and shape in C-28 than in PI 193407. R. solani penetrated C-28 fruit by means of numerous infection pegs emanating from infection cushions, whereas in PI 193407 penetration was by individual hyphae. The establishment of R. solani in both hosts involved inter- and intracellular growth and the subsequent destruction of epidermal and subepidermal layers of cells. However, advancement of the pathogen in all tissues was slower in the resistant than in the susceptible host. Infected resistant parenchyma tissues stained more intensely with safranin O than did those of the susceptible host. This suggested that a chemical substance(s) may be responsible for “walling-off” the organism or slowing lesion development in the resistant host. In addition, the cell walls in PI 193407 dissolved in advance of hyphae of the pathogen, which resulted in microcavities in the carpel wall.