Abstract

Differential growth of various strains of Ceratocystis fimbriata was demonstrated in an extract from sweet potato infected by a sweet potato strain. Mycelial growth and spore germination of the sweet potato strain, pathogenic to sweet potato, was slightly inhibited in the infected tissue extract, whereas mycelial growth and spore germination of non-pathogenic strains from coffee, prune, cacao, oak, taro and almond were severely inhibited, with the exception of spore germination by the cacao strain. Furanoterpenoids (mainly ipomeamarone, dehydroipomeamarone and ipomeamaronol) were shown to be the main cause of the differential inhibitory activity of the infected tissue extract. There were differences in the depth of cell layers containing the accumulated furanoterpenoids, and in their concentration per disk, among the tissues infected by the various strains of the fungus. The depth of accumulation of furanoterpenoids and their concentration per disk of tissue infected by the sweet potato strain were greater than in tissues infected by all other non-pathogenic strains. All concentrations of furanoterpenoids in the tissues infected by the seven strains appeared to be high enough to inhibit growth of the fungi. When furanoterpenoid production of sweet potato root tissue was inhibited by treatment with cycloheximide, the coffee strain, which is naturally non-pathogenic to sweet potato, behaved as a pathogenic fungus on the tissue.

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