VIEW ARTICLE

Physiology and Biochemistry

Effects of Dihydrofusarubin and Isomarticin from Fusarium solani on Carbohydrate Status and Metabolism of Rough Lemon Seedlings. S. Nemec, Plant pathologist, U.S. Department of Agriculture, Agricultural Research Service, U.S. Horticultural Research Laboratory, Orlando, FL 32803; D. Phelps(2), and R. Baker(3). (2)Research associate, U.S. Department of Agriculture, Agricultural Research Service, U.S. Horticultural Research Laboratory, Orlando, FL 32803; (3)Chemist, U.S. Department of Agriculture, Agricultural Research Service, U.S. Citrus and Subtropical Products Laboratory, Winter Haven, FL 33880. Phytopathology 79:700-705. Accepted for publication 16 February 1989. 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, 1989. DOI: 10.1094/Phyto-79-700.

Rough lemon citrus seedlings inoculated with Fusarium solani and seedlings suspended with their roots in solutions of the F. solani-produced naphthoquinones dihydrofusarubin (DHF, 100 mg L^–1) and isomarticin (50 mg L^–1) developed similar wilt symptoms. Only those seedlings treated with DHF developed chlorosis symptoms. Total soluble and reducing sugars and starch were reduced in inoculated plants, but only starch was consistently reduced in naphthoquinone-treated plants. Total protein did not differ between inoculated plants, naphthoquinone-treated plants, and their controls. DHF-treated plants were evaluated for chlorophylls a and b and ATPase activity, and no differences were present in the treated versus the control plants. In general, naphthoquinone-treated plants, as well as inoculated plants, accumulated more minerals in leaves than did control plants. Respiration increased in DHF-treated plants both in a greenhouse and in a growth chamber. This respiration response was studied in growth chamber experiments with the inhibitors dinitrophenol, sodium azide, salicylhydroxamic acid, and sodium fluoride. These studies suggested that respiration is stimulated via mitochondrial oxidases.