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Resistance

Effect of Resistance on Growth of Cercospora beticola Race C2 on the Leaf Surface and within Leaf Tissue of Sugar Beet. E. D. Whitney, Plant pathologist, Agricultural Research, Science and Education Admimistration, U.S. Department of Agriculture, U.S. Agricultural Research Station, Salinas, CA 93915; N. F. Mann, biological technician, Agricultural Research, Science and Education Admimistration, U.S. Department of Agriculture, U.S. Agricultural Research Station, Salinas, CA 93915. Phytopathology 71:633-638. Accepted for publication 17 November 1980. This article is in the public domain and not copyrightable. It may be freely reprinted with customary crediting of the source. The American Phytopathological Society, 1981. DOI: 10.1094/Phyto-71-633.

When the open-pollinated sugar beet cultivar FC 701/2 was inoculated with Cercospora beticola, race C2, individual plants responded with either a susceptible reaction, a large fleck reaction, a small fleck reaction, or no visible reaction. For a given plant, these symptoms were consistent from one time of inoculation to another. On resistant plants, the number of germ tubes per conidium, width of mycelium, and appressorium length were reduced, and the appressorium configuration was altered, compared to those parameters on susceptible plants. We interpret these changes as a fungal response to the resistance of the plants rather than as an environmental effect. Histopathological studies showed that, although not usually visible to the unaided eye, necrosis of host tissue was present at or near the site of hyphal penetration about one third the depth of the leaf thickness. The amount of necrosis was similar in the large and small fleck host response. The hyphae within the resistant host were usually limited to a single mycelium with one or two branches, while in the susceptible hosts a dense stroma developed in the necrotic tissue. Chloroplasts, nuclei, and nucleoli were degenerate in infected cells near hyphae compared with those from healthy cells.

Additional keywords: host-parasite relationship, genetic variation, Beta vulgaris.