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Mutational Analysis of Gliotoxin Production by the Biocontrol Fungus Gliocladium virens in Relation to Suppression of Pythium Damping-off. Stephen E. Wilhite, Department of Botany and Agricultural Experiment Station, University of Maryland, College Park 20742; Robert D. Lumsden(2), and David C. Straney(3). (2)Biocontrol of Plant Disease Laboratory, USDA/ARS, Beltsville, MD 20705; (3)Department of Botany and Agricultural Experiment Station, University of Maryland, College Park 20742. Phytopathology 84:816-821. Accepted for publication 25 April 1994. 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, 1994. DOI: 10.1094/Phyto-84-816.

The fungus Gliocladium virens is an important biocontrol agent against plant pathogenic fungi, such as Pythium ultimum and Rhizoctonia solani, that cause damping-off diseases. G. virens strain G20 (synonym GL21) has been commercially formulated into the disease-suppressing product Gliogard (W. R. Grace & Co., CT). One possible mechanism of G. virens biocontrol may be the production of the fungistatic metabolite gliotoxin. The presence of this metabolite has been associated previously with disease suppressive activity toward P. ultimum. The purpose of this study was to critically test, using mutational analysis, the importance of gliotoxin production in the disease-suppressiveness effected against P. ultimum. Seven mutants lacking gliotoxin production (Glx phenotype) were isolated by selection-based enrichment and screening procedures following UV-treatment of parental strain G20-4VIB (WT). On average, these Glx mutants displayed only 54% of the disease-suppressive activity of the wild-type isolate in vivo and experienced a nearly total loss of antagonistic activity in vitro toward P. ultimum. This study represents strong genetic evidence supporting a major role for antibiosis in the suppression of a plant disease by a fungal biocontrol agent.

Additional keywords: fungal metabolite.