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Some Biochemical Factors Associated with the Infection of Cotton Fruit by Diplodia gossypina. Sy-ying C. Wang, Postdoctoral Fellow, Agricultural Experiment Station, Louisiana State University, Baton Rouge 70803; J. A. Pinckard, Professor, Agricultural Experiment Station, Louisiana State University, Baton Rouge 70803. Phytopathology 62:460-465. Accepted for publication 18 November 1971. DOI: 10.1094/Phyto-62-460.

Germinating spores and mycelium of Diplodia gossypina on the surfaces of the immature fruit of cotton, Gossypium hirsutum ‘Deltapine 16’, caused the necrosis and death of certain epidermal cells within 48 to 72 hr after inoculation. The first epidermal cells injured were the guard cells of stomata, their subsidiary cells, and multicellular epidermal hairs. These symptoms were reproduced by treating bolls with extracts of rotted carpel wall tissue, commercial polygalacturonase, cellulase, and cell-free culture filtrates of D. gossypina grown on synthetic media containing pectin, carboxymethylcellulose, glucose, and lecithin and on cotton boll tissue medium. Cell injury was substantially reduced after the culture filtrates were heated. Culture filtrates containing pectic enzymes and commercial polygalacturonase were the most active in producing cell necrosis. Glucose, fructose, galactose, sucrose, raffinose, and two unidentified materials were found present in the nectar and the washings from normal boll surfaces. Cellulase, cellobiase, xylanase, arabanase, proteases, and phosphatidases were found in extracts of rotted tissues. Active tissue maceration paralleled optimal conditions for polygalacturonate trans-eliminase activity. The fungus first predisposes the thin-walled cells surrounding the stomata to invasion by enzymatic and toxic action in advance of hyphal penetration. Exopolygalacturonase is suspected of being a dominant enzyme responsible for the primary symptoms of cotton boll rot caused by D. gossypina.

Additional keywords: disease resistance.