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Repression of Virulence in Rhizoctonia solani by Glucose and 3-O-Methyl Glucose. A. R. Weinhold, Professor, Department of Plant Pathology, University of California, Berkeley 94720; Tully Bowman, Staff Research Associate, Department of Plant Pathology, University of California, Berkeley 94720. Phytopathology 64:985-990. Accepted for publication 11 February 1974. DOI: 10.1094/Phyto-64-985.

An exogenous source of glucose resulted in reduced virulence of Rhizoctonia solani on 5-day-old cotton seedlings. Lesion areas were 32.5, 7.8, and 4.1 mm2 after treatment with solutions of 14, 28, and 56 mM glucose, respectively, compared with 82.0 mm2 for water controls. A solution of 28 mM glucose prevented the production of pectinase by R. solani in vitro. Other sugars were tested and, with the exception of arabinose, there was a direct relationship between utilization by R. solani as a source of carbon, inhibition of disease development, and repression of pectinase. Arabinose was a relatively poor carbon source for growth, and was only partially effective in reducing disease development. It did, however, repress pectinase production in the in vitro system. Disease development was also prevented by a solution of 5.2 mM 3-O-methyl glucose (MeG). In contrast to glucose MeG was active at lower concns and enhanced pectinase production in vitro. Growth of R. solani was reduced by MeG but this effect was overcome by the addition of a small quantity of glucose. In the presence of glucose infection cushions formed but the typical R. solani lesion did not develop. With MeG, however, the pathogen grew on the hypocotyl, but infection cushions were not formed. Combinations of glucose and MeG increased mycelial growth on the hypocotyl, but did not result in infection cushion formation. Glucose appears to interfere with disease development through prevention of tissue maceration by pectinolytic enzymes, whereas MeG appears to interfere with processes that lead to infection cushion formation.

Additional keywords: cotton, seedling disease, catabolite repression.